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1
Paramanantham, Anjugam, Eun Joo Jung, Se-IL Go, Bae Kwon Jeong, Jin-Myung Jung, Soon Chan Hong, Gon Sup Kim, and Won Sup Lee. "Activated ERK Signaling Is One of the Major Hub Signals Related to the Acquisition of Radiotherapy-Resistant MDA-MB-231 Breast Cancer Cells." International Journal of Molecular Sciences 22, no. 9 (May 6, 2021): 4940. http://dx.doi.org/10.3390/ijms22094940.
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Breast cancer is one of the major causes of deaths due to cancer, especially in women. The crucial barrier for breast cancer treatment is resistance to radiation therapy, one of the important local regional therapies. We previously established and characterized radio-resistant MDA-MB-231 breast cancer cells (RT-R-MDA-MB-231 cells) that harbor a high expression of cancer stem cells (CSCs) and the EMT phenotype. In this study, we performed antibody array analysis to identify the hub signaling mechanism for the radiation resistance of RT-R-MDA-MB-231 cells by comparing parental MDA-MB-231 (p-MDA-MB-231) and RT-R-MDA-MB-231 cells. Antibody array analysis unveiled that the MAPK1 protein was the most upregulated protein in RT-R-MDA-MB-231 cells compared to in p-MDA-MB-231 cells. The pathway enrichment analysis also revealed the presence of MAPK1 in almost all enriched pathways. Thus, we used an MEK/ERK inhibitor, PD98059, to block the MEK/ERK pathway and to identify the role of MAPK1 in the radio-resistance of RT-R-MDA-MB-231 cells. MEK/ERK inhibition induced cell death in both p-MDA-MB-231 and RT-R-MDA-MB-231 cells, but the death mechanism for each cell was different; p-MDA-MB-231 cells underwent apoptosis, showing cell shrinkage and PARP-1 cleavage, while RT-R-MDA-MB-231 cells underwent necroptosis, showing mitochondrial dissipation, nuclear swelling, and an increase in the expressions of CypA and AIF. In addition, MEK/ERK inhibition reversed the radio-resistance of RT-R-MDA-MB-231 cells and suppressed the increased expression of CSC markers (CD44 and OCT3/4) and the EMT phenotype (β-catenin and N-cadherin/E-cadherin). Taken together, this study suggests that activated ERK signaling is one of the major hub signals related to the radio-resistance of MDA-MB-231 breast cancer cells.
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Jin, Hana, Young Shin Ko, Sang Won Park, Ki Churl Chang, and Hye Jung Kim. "13-Ethylberberine Induces Apoptosis through the Mitochondria-Related Apoptotic Pathway in Radiotherapy-Resistant Breast Cancer Cells." Molecules 24, no. 13 (July 4, 2019): 2448. http://dx.doi.org/10.3390/molecules24132448.
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Berberine is reported to have multiple biological effects, including antimicrobial, anti-inflammatory, and antitumor activities, and 13-alkyl-substituted berberines show higher activity than berberine against certain bacterial species and human cancer cell lines. In particular, 13-ethylberberine (13-EBR) was reported to have anti-inflammatory effects in endotoxin-activated macrophage and septic mouse models. Thus, in this study, we aimed to examine the anticancer effects of 13-EBR and its mechanisms in radiotherapy-resistant (RT-R) MDA-MB-231 cells derived from the highly metastatic MDA-MB-231 cells. When we compared the gene expression between MDA-MB-231 and RT-R MDA-MB-231 cells with an RNA microarray, RT-R MDA-MB-231 showed higher levels of anti-apoptotic genes and lower levels of pro-apoptotic genes compared to MDA-MB-231 cells. Accordingly, we examined the effect of 13-EBR on the induction of apoptosis in RT-R MDA-MB-231 and MDA-MB-231 cells. The results showed that 13-EBR reduced the proliferation and colony-forming ability of both MDA-MB-231 and RT-R MDA-MB-231 cells. Moreover, 13-EBR induced apoptosis by promoting both intracellular and mitochondrial reactive oxygen species (ROS) and by regulating the apoptosis-related proteins involved in the intrinsic pathway, not in the extrinsic pathway. These results suggest that 13-EBR has pro-apoptotic effects in RT-R MDA-MB-231 and MDA-MB-231 cells by inducing mitochondrial ROS production and activating the mitochondrial apoptotic pathway, providing useful insights into new potential therapeutic strategies for RT-R breast cancer treatment.
3
Yuan, Fahu, Xinghua Liao, and Tongcun Zhang. "Nobiletin enhances Pirarubicin chemosensitivity of breast cancer cell MDA-MB-231 by regulating PER2." E3S Web of Conferences 233 (2021): 02010. http://dx.doi.org/10.1051/e3sconf/202123302010.
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To explore the potential mechanism of nobiletin in improving the sensitivity of breast cancer MDA-MB-231 cells to Pirarubicin. MDA-MB-231 cells were randomly divided into Control group, Nobiletin group, Pirarubicin group and Nobiletin co-Pirarubicin group. CCK-8 assay was used to detect the inhibitory effect of Nobiletin co-Pirarubicin on the proliferation of MDA-MB-231 cells, and the cell cycle and apoptosis of MDA-MB-231 cells were detected by flow cytometry. The effect of nobiletin combined with Pirarubicin on the migration and repair ability of MDA-MB-231 cells was detected by scratch test. Western blotting was used to determine the effect of nobiletin co-Pirarubicin on Period2 (PER2), apoptosis-related proteins Bax and BCL-2 expression levels in MDA-MB-231 cells. The results showed that the sensitivity of MDA-MB-231 cells to Pirarubicin was enhanced by nobiletin. Compared with Pirarubicin or nobiletin alone, Pirarubicin combined with nobiletin promoted the apoptosis of MDA-MB-231 cells and the expression of apoptosis-related protein Bax, and reduced the expression of apoptosis-inhibiting protein BCL-2. The combination of nobiletin and Pirarubicin significantly inhibited the proliferation and promoted the apoptosis of MDA-MB-231 cells, which may be mediated by the enhancement of PER2 expression by nobiletin.
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Ko, Young Shin, Trojan Rugira, Hana Jin, Young Nak Joo, and Hye Jung Kim. "Radiotherapy-Resistant Breast Cancer Cells Enhance Tumor Progression by Enhancing Premetastatic Niche Formation through the HIF-1α-LOX Axis." International Journal of Molecular Sciences 21, no. 21 (October 28, 2020): 8027. http://dx.doi.org/10.3390/ijms21218027.
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Cancer stem cells (CSCs) exist in solid tumors and contribute to therapeutic resistance and disease recurrence. Previously, we reported that radiotherapy-resistant (RT-R)-MDA-MB-231 cells from highly metastatic MDA-MB-231 cells produced more CSCs than any other RT-R-breast cancer cells and showed therapeutic resistance and enhanced invasiveness. Hypoxia inducible factor-1α (HIF-1α) induced in the tumor microenvironment leads to the release of lysyl oxidase (LOX), which mediates collagen crosslinking at distant sites to facilitate environmental changes that allow cancer cells to easily metastasize. Therefore, in this study, we investigated whether RT-R-MDA-MB-231 cells induce greater HIF-1α expression, LOX secretion, and premetastatic niche formation than MDA-MB-231 cells do. RT-R-MDA-MB-231 cells increased HIF-1α expression and LOX secretion compared with MDA-MB-231 cells. Mice harboring RT-R-MDA-MB-231 cell xenografts showed enhanced tumor growth and higher expression of the CSC markers, CD44, Notch-4, and Oct3/4. In addition, mice injected with RT-R-MDA-MB-231 cells exhibited a higher level of HIF-1α in tumor tissue, increased secretion of LOX in plasma, higher induced levels of crosslinked collagen, and a higher population of CD11b+ BMDC recruitment around lung tissue, compared with those injected with MDA-MB-231 cells. These results suggest that RT-R-MDA-MB-231 cells contribute to tumor progression by enhancing premetastatic niche formation through the HIF-1α-LOX axis.
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Yang, Ji, Yue Wu, Xiao Wang, Liqian Xu, Xiaohong Zhao, and Yunmei Yang. "Chemoresistance is associated with overexpression of HAX-1, inhibition of which resensitizes drug-resistant breast cancer cells to chemotherapy." Tumor Biology 39, no. 3 (March 2017): 101042831769222. http://dx.doi.org/10.1177/1010428317692228.
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Acquired resistance to standard chemotherapy is the common and critical limitation for cancer therapy. Hematopoietic cell-specific protein 1-associated protein X-1 (HAX-1) has been reported to be upregulated in numerous cancers. However, the role of HAX-1 in oncotherapy remains unclear. In this study, we established MDA-MB-231 cell lines which were resistant to cisplatin (MDA-MB-231/CR) or doxorubicin (MDA-MB-231/DR) to study the chemoresistance in breast cancer. As a result, the HAX-1 which is an apoptosis-associated protein was observed to be overexpressed in both MDA-MB-231/CR and MDA-MB-231/DR compared with the routine MDA-MB-231 cells. Moreover, knockdown of HAX-1 via RNA interference decreased IC50 level of cisplatin by 70.91% in MDA-MB-231/CR cells, and the IC50 level of doxorubicin was decreased by 76.46% in MDA-MB-231/DR cells when the HAX-1 was downregulated. Additionally, we found that the knockdown of HAX-1 induced the release of cytochrome C from mitochondria, resulting in the activation of caspases. Taken together, our study indicates that the overexpression of HAX-1 is essential in the development of chemoresistance in breast cancer. Furthermore, we identify that HAX-1 may become the target for cancer therapy.
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Risha, Y., V. Susevski, N. Hüttmann, S. Poolsup, Z. Minic, and M. V. Berezovski. "Proteome of breast cancer derived microvesicles." Siberian Medical Review, no. 2 (2021): 68–71. http://dx.doi.org/10.20333/25000136-2021-2-68-71.
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The aim of the research. To examine the proteomic profi le of breast cancer exosomes. Material and methods. Cell lines used for this study were MDA-MB-231 female epithelial breast cancer cells (ATCC HTB-26) and MCF10A non-tumorigenic epithelial breast tissue cells. MVs were isolated using diff erential ultracentrifugation. Samples were lysed, reduced, alkylated, digested, and analyzed by an Orbitrap Fusion mass spectrometer. MS raw fi les were analyzed using MaxQuant version 1.6.12.0. Peptides were searched against the human UniProt FASTA database using the Andromeda search engine, integrated into MaxQuant. Results. MVs derived from MCF10A and MDA-MB-231 cell lines were analyzed, and 1427 and 547 proteins were identifi ed in the MDA-MB-231 and MCF10A-derived MVs, respectively. In total, 455 proteins were common to both MDA-MB-231 and MCF10A MVs. MVs derived from MCF10A and MDAMB-231 cell lines were analyzed, and 1427 and 547 proteins were identifi ed in the MDA-MB-231 and MCF10A-derived MVs, respectively. In total, 455 proteins were common to both MDA-MB-231 and MCF10A MVs. Th e unique MDA-MB-231 MV proteins were searched against the DisGeNET human diseases database. Out of 972 MDA-MB-231 MV proteins, 112 were cancer-related while 32 were specifi cally associated with BC. In the MDA-MB-231 MV proteome, 23 Wnt signaling pathway proteins were identifi ed based on their GO biological process. Proteomic analysis identifi ed enzymes OAT, TALDO1, and BLMH were only in MVs from metastatic MDA-MB-231 cell line. The specific activity of OAT and TALDO1 was higher in MV fractions of MDA-MB-231 in comparison to the non-cancerous MCF10A cell line-derived MVs. Th ese fi ndings might suggest that these enzymes might play a role in BC. In our present study, we found that some enzymes identifi ed from MV fractions were already proposed to play a role in cancer therapy as therapeutic targets (OAT, TALDO1) and resistance against chemotherapy agents (BLMH).
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Trieu, V., S. Ran, C. Bivens, and N. Desai. "Chemoprotection by VEGF: Rationale for combination nab-paclitaxel and bevacizumab." Journal of Clinical Oncology 25, no. 18_suppl (June 20, 2007): 1064. http://dx.doi.org/10.1200/jco.2007.25.18_suppl.1064.
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1064 Background: Nanoparticle albumin-bound (nab-) paclitaxel (ABX) has shown greater efficacy and less toxicity than solvent-based paclitaxel (TAX) in xenograft models and clinical trials. The goal of this study was to determine the effects of VEGF modulation in human MDA-MB-231 breast tumor cell line and the effects of ABX and VEGF-neutralizing antibody bevacizumab (AVA) combination on the growth and metastasis of orthotopically implanted MDA-MB-231 tumors. Methods: VEGF expression was evaluated by ELISA in MDA-MB-231 tumor extract one week after treatment (qdx5) with saline, doxorubicin (10 mg/kg), TAX (10 mg/kg), or ABX (15 mg/kg). VEGF-receptor expression in MDA-MB-231 was quantitated by RT-PCR. MDA-MB-231 cytotoxicity with ABX, VEGF, AVA alone or in combination was measured by cytotoxicity and clonogenic assays. Implanted MDA-MB-231 tumors expressing luciferase were treated with saline, 2 cycles of ABX (10 mg/kg, two qdx5 cycles separated by 1 week, N=5) alone or in combination with AVA (2, 4 and 8 mg/kg, 2/wkx6). Tumor lymph node and pulmonary metastasis was determined by measuring luciferase activity. Results: Compared with saline, MDA-MB-231 tumors following chemotherapies exhibited significant tumor shrinkage (p≤0.006, t-test) and VEGF induction (p<0.0001, t-test). MDA-MB-231 was shown to express VEGFR2. Exogenous VEGF had a protective effect on MDA-MB-231 tumor cells by reducing cytotoxicity of ABX in both cytotoxicity and clonogenic assays. Sequestration of VEGF with AVA increased cytotoxicity of ABX in vitro. Treatment of MDA-MB-231 breast tumors with ABX and AVA combination resulted in greater than additive antitumor response and significantly reduced metastasis to the lungs (p=0.025 vs control) and LN (p=0.022) at the highest AVA dose. Conclusions: Chemotherapies induced VEGF expression in MDA-MD-231 breast tumor in vivo. In vitro, VEGF exerted a protective effect against ABX chemotherapy in VEGFR2-expressing MDA-MD-231 cells, which was abrogated by addition of AVA. In vivo, ABX and AVA combination significantly inhibited the metastatic potential of MDA-MB-231 tumor cells. These data provide a rational basis for the combination of nab- paclitaxel and bevacizumab in VEGF-receptor expressing tumors. [Table: see text]
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Lee, Hwan Hee, Joohee Jung, Aree Moon, Hyojeung Kang, and Hyosun Cho. "Antitumor and Anti-Invasive Effect of Apigenin on Human Breast Carcinoma through Suppression of IL-6 Expression." International Journal of Molecular Sciences 20, no. 13 (June 27, 2019): 3143. http://dx.doi.org/10.3390/ijms20133143.
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Interleukin (IL)-6 plays a crucial role in the progression, invasion, and metastasis of breast cancer. Triple-negative breast cancer (TNBC) cell line MDA-MB-231 is known for its aggressive metastasis. Epithelial to mesenchymal transition (EMT) is a critical process in cancer metastasis. The positive correlation between IL-6 and EMT in tumor microenvironment is reported. We found significantly upregulated IL-6 expression in MDA-MB-231 cells. A blockade of IL-6 expression decreased levels of phosphorylated signal transducer and activator of transcription 3 (pSTAT3), phosphatidylinositol-4,5-bisphosphate 3-kinase (PI3K), phosphorylated protein kinase B (pAkt), and cell cycle-related molecules, including cyclin-dependent kinases (CDKs) and cyclins in MDA-MB-231 cells. A short-hairpin RNA (shRNA)-mediated blockade of IL-6 expression inhibited migration and N-cadherin expression and induced E-cadherin expression in MDA-MB-231 cells. Growth rate was slower for the tumors derived from IL-6 shRNA-treated MDA-MB-231 cells than for those derived from control shRNA-treated MDA-MB-231 cells. The expression of pSTAT3, phosphorylated extracellular signal-regulated kinase (pERK), PI3K, pAkt, snail, vimentin, and N-cadherin was significantly lower in tumors from IL-6 shRNA-treated MDA-MB cells. In addition, apigenin treatment significantly inhibited the growth of MDA-MB-231-derived xenograft tumors along with the protein expressions of pSTAT3, pERK, IL-6, PI3K, pAkt, and N-cadherin. Our results demonstrate that the anti-invasive effect of apigenin in MDA-MB-231-derived xenograft tumors is mediated by the inhibition of IL-6-linked downstream signaling pathway.
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Alva, A. S., Z. Varsos, H. Roca, and K. Pienta. "Effect of CCL2 on survival of breast cancer MDA-MB-231 cells via inhibition of apoptosis." Journal of Clinical Oncology 27, no. 15_suppl (May 20, 2009): e22176-e22176. http://dx.doi.org/10.1200/jco.2009.27.15_suppl.e22176.
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e22176 Background: The cytokine CCL2 (Chemokine (C-C) motif ligand 2 or monocyte chemo attractant protein-1 MCP-1) has been shown to play an important role in breast cancer progression by promoting angiogenesis and migration. CCL2 is over-expressed by breast cancer cells as well as by macrophages and mesenchymal stem cells in the tumor micro-environment. We studied the effects of CCL2 and IL-6 on survival of breast cancer MDA-MB-231 cells. Methods: Cytokine expression including of CCL2 and IL- 6 were analyzed in supernatants from MDA-MB-231 cells using cytokine antibody array (Human Antibody Array 3; Ray Biotech, Inc). Serum starved MDA-MB-231 cells were treated with CCL2 (75 ng/mL) and IL-6 (100 ng/mL; both from Apollo Cytokine Research). Cell viability in response to treatment was analyzed at serial time points by cell proliferation assay WST-1 (Roche Applied Science). Protein expression of genes of interest was studied by Western blot. Results: In contrast to primary breast tumor cells, MDA-MB-231 cells express minimal CCL2 at baseline. MDA-MB-231 cells also exhibit low expression of IL-6. Stimulation of MDA-MB-231 cells with either exogenous CCL2 or exogenous IL-6 did not increase levels of the other cytokine. In MDA-MB-231 cells, CCL2, alone and in combination with IL-6, promotes survival in serum starved conditions. Treatment of MDA-MB-231 cells with CCL2 leads to survivin up-regulation beginning at 48 hours as determined by immunoblotting analysis. CCL2 in combination with IL-6 inhibits the cleavage of PARP, lamin and caspase3. Conclusions: There is minimal endogenous expression of CCL2 in MDA-MB-231 cells. CCL2 from the tumor micro-environment promotes survival of MDA-MB-231 cells associated with up-regulation of survivin. IL-6 may play a syngeristic role with CCL2 in promoting survival of MDA-MB-231 cells. We plan to explore the role of survivin up-regulation in protecting cells from cell death. Our findings raise the possibility of utilizing neutralizing antibodies against CCL2 in therapy of breast cancer. No significant financial relationships to disclose.
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Jin, Hana, Trojan Rugira, Young Shin Ko, Sang Won Park, Seung Pil Yun, and Hye Jung Kim. "ESM-1 Overexpression is Involved in Increased Tumorigenesis of Radiotherapy-Resistant Breast Cancer Cells." Cancers 12, no. 6 (May 26, 2020): 1363. http://dx.doi.org/10.3390/cancers12061363.
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The key barrier to the effectiveness of radiotherapy remains the radioresistance of breast cancer cells, resulting in increased tumor recurrence and metastasis. Thus, in this study, we aimed to clarify the difference between radiotherapy-resistant (RT-R) breast cancer (BC) and BC, and accordingly, analyzed gene expression levels between radiotherapy-resistant (RT-R) MDA-MB-231 cells and MDA-MB-231 cells. Gene expression array showed that ESM-1 was the most upregulated in RT-R-MDA-MB-231 cells compared to MDA-MB-231 cells. Then, we aimed to investigate the role of ESM-1 in the increased tumorigenesis of RT-R-BC cells. RT-R-MDA-MB-231, which showed an increased expression level of ESM1, exhibited significantly enhanced proliferation, colony forming ability, migration, and invasion compared to MDA-MB-231 cells, and ESM-1 knockdown effectively reversed these effects. In addition, compared to MDA-MB-231 cells, RT-R-MDA-MB-231 cells displayed improved adhesion to endothelial cells (ECs) due to the induction of adhesion molecules and increased MMP-9 activity and VEGF-A production, which were decreased by ESM-1 knockdown. Moreover, the expression of HIF-1α and activation of NF-κB and STAT-3 were increased in RT-R-MDA-MB-231 cells compared to MDA-MB-231 cells, and these effects were abolished by the knockdown of ESM-1. Finally, we confirmed the role of ESM-1 in tumorigenesis in an in vivo mouse model. Tumor volume, lung metastasis, and tumorigenic molecules (VEGF-A, HIF-1α, MMP-9, ICAM-1, VCAM-1, and phospho-NF-κB and phospho-STAT-3) were significantly induced in mice injected with ESM-1-overexpressing 4T1 cells and greatly enhanced in those injected with ESM-1-overexpressing RT-R-4T1 cells. Taken together, these results suggest for the first time that ESM-1 plays a critical role in tumorigenesis of breast cancer cells, especially RT-R-breast cancer cells, through the induction of cell proliferation and invasion.
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Zarà, Marta, Gianni Guidetti, Daniela Boselli, Chiara Villa, Ilaria Canobbio, Claudio Seppi, Caterina Visconte, Jessica Canino, and Mauro Torti. "Release of Prometastatic Platelet-Derived Microparticles Induced by Breast Cancer Cells: A Novel Positive Feedback Mechanism for Metastasis." TH Open 01, no. 02 (July 2017): e155-e163. http://dx.doi.org/10.1055/s-0037-1613674.
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AbstractCirculating platelets and platelet-derived microparticles are regulators of cancer metastasis. In this study, we show that breast cancer cells induce platelet aggregation and lead to the release of platelet-derived microparticles. Although able to cause comparable aggregation, the highly aggressive MDA-MB-231 cells were more potent than the poorly aggressive MCF7 cells in inducing platelet-derived microparticles release, which was comparable to that promoted by thrombin. MDA-MB-231 cells were able to bind and internalize both MCF7- and MDA-MB-231-induced platelet-derived microparticles with comparable efficiency. By contrast, MCF7 cells did not interact with either type of platelet-derived microparticles. Upon internalization, only platelet-derived microparticles released by platelet stimulation with MDA-MB-231 cells, but not those released upon stimulation with MCF7 cells, caused activation of MDA-MB-231 cells and promoted the phosphorylation of selected signaling proteins, including p38MAPK and myosin light chain. Accordingly, MDA-MB-231-induced, but not MCF7-induced, platelet-derived microparticles dose-dependently stimulated migration and invasion of targeted MDA-MB-231 cells. These results identify a novel paracrine positive feedback mechanism initiated by aggressive breast cancer cell types to potentiate their invasive phenotype through the release of platelet-derived microparticles.
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Levine, Fayola, and Olorunseun O. Ogunwobi. "Targeting PVT1 Exon 9 Re-Expresses Claudin 4 Protein and Inhibits Migration by Claudin—Low Triple Negative Breast Cancer Cells." Cancers 13, no. 5 (March 2, 2021): 1046. http://dx.doi.org/10.3390/cancers13051046.
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PVT1 is a long non-coding RNA transcribed from a gene located at the 8q24 chromosomal region that has been implicated in multiple cancers including breast cancer (BC). Amplification of the 8q24 chromosomal region is a common event in BC and is associated with poor clinical outcomes. Claudin–low (CL) triple negative breast cancer (TNBC) is a subtype of BC with a particularly dismal outcome. We assessed PVT1 exon 9 expression in the T47D estrogen receptor positive BC cell line, and in the MDA MB 468 and MDA MB 231 TNBC cell lines, followed by the assessment of the expression of claudins 1, 3, 4 and 7, in MDA MB 468 and MDA MB 231 (TNBC) cells. We found that MDA MB 231 TNBC cells significantly express less claudin 1, 3, 4, and 7 than MDA MB 468 TNBC cells. PVT1 exon 9 is significantly upregulated in MDA MB 231 CL TNBC cells, and significantly downregulated in MDA MB 468 claudin high (CH) TNBC cells, in comparison to T47D estrogen receptor positive BC cells. We then analyzed the functional consequences of siRNA targeting of PVT1 exon 9 expression in the MDA MB 231 CL TNBC cells. Notably, siRNA targeting of PVT1 exon 9 expression in the MDA MB 231 CL TNBC cells led to a significant reduction in migration and the re-expression of claudin 4. Taken together, our data indicate that PVT1 exon 9 regulates claudin 4 expression and migration in CL TNBC cells, and may have clinical implications in CL TNBC.
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Ko, Young Shin, Eun Joo Jung, Se-il Go, Bae Kwon Jeong, Gon Sup Kim, Jin-Myung Jung, Soon Chan Hong, Choong Won Kim, Hye Jung Kim, and Won Sup Lee. "Polyphenols Extracted from Artemisia annua L. Exhibit Anti-Cancer Effects on Radio-Resistant MDA-MB-231 Human Breast Cancer Cells by Suppressing Stem Cell Phenotype, β-Catenin, and MMP-9." Molecules 25, no. 8 (April 21, 2020): 1916. http://dx.doi.org/10.3390/molecules25081916.
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Artemisia annua L. has been reported to show anti-cancer activities. Here, we determined whether polyphenols extracted from Artemisia annua L. (pKAL) exhibit anti-cancer effects on radio-resistant MDA-MB-231 human breast cancer cells (RT-R-MDA-MB-231 cells), and further explored their molecular mechanisms. Cell viability assay and colony-forming assay revealed that pKAL inhibited cell proliferation on both parental and RT-R-MDA-MB-231 cells in a dose-dependent manner. The anti-proliferative effects of pKAL on RT-R-MDA-MB-231 cells were superior or similar to those on parental ones. Western blot analysis revealed that expressions of cluster of differentiation 44 (CD44) and Oct 3/4, matrix metalloproteinase-9 (MMP-9) and signal transducer and activator of transcription-3 (STAT-3) phosphorylation were significantly increased in RT-R-MDA-MB-231 cells compared to parental ones, suggesting that these proteins could be associated with RT resistance. pKAL inhibited the expression of CD44 and Oct 3/4 (CSC markers), and β-catenin and MMP-9 as well as STAT-3 phosphorylation of RT-R-MDA-MB-231. Regarding upstream signaling, the JNK or JAK2 inhibitor could inhibit STAT-3 activation in RT-R-MDA-MB-231 cells, but not augmented pKAL-induced anti-cancer effects. These findings suggest that c-Jun N-terminal kinase (JNK) or Janus kinase 2 (JAK2)/STAT3 signaling are not closely related to the anti-cancer effects of pKAL. In conclusion, this study suggests that pKAL exhibit anti-cancer effects on RT-R-MDA-MB-231 cells by suppressing CD44 and Oct 3/4, β-catenin and MMP-9, which appeared to be linked to RT resistance of RT-R-MDA-MB-231 cells.
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Adinew, Getinet M., Samia S. Messeha, Equar Taka, Ramesh B. Badisa, Lovely M. Antonie, and Karam F. A. Soliman. "Thymoquinone Alterations of the Apoptotic Gene Expressions and Cell Cycle Arrest in Genetically Distinct Triple-Negative Breast Cancer Cells." Nutrients 14, no. 10 (May 19, 2022): 2120. http://dx.doi.org/10.3390/nu14102120.
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Breast cancer (BC) is the most common cancer in women worldwide, and it is one of the leading causes of cancer death in women. triple-negative breast Cancer (TNBC), a subtype of BC, is typically associated with the highest pathogenic grade and incidence in premenopausal and young African American (AA) women. Chemotherapy, the most common treatment for TNBC today, can lead to acquired resistance and ineffective treatment. Therefore, novel therapeutic approaches are needed to combat medication resistance and ineffectiveness in TNBC patients. Thymoquinone (TQ) is shown to have a cytotoxic effect on human cancer cells in vitro. However, TQ’s mode of action and precise mechanism in TNBC disease in vitro have not been adequately investigated. Therefore, TQ’s effects on the genetically different MDA-MB-468 and MDA-MB-231 human breast cancer cell lines were assessed. The data obtained show that TQ displayed cytotoxic effects on MDA-MB-468 and MDA-MB-231 cells in a time- and concentration-dependent manner after 24 h, with IC50 values of 25.37 µM and 27.39 µM, respectively. Moreover, MDA-MB-231 and MDA-MB-468 cells in a scratched wound-healing assay displayed poor wound closure, inhibiting invasion and migration via cell cycle blocking after 24 h. TQ arrested the cell cycle phase in MDA-MB-231 and MDA-MB-468 cells. The three cell cycle stages in MDA-MB-468 cells were significantly affected at 15 and 20 µM for G0/G1 and S phases, as well as all TQ concentrations for G2/M phases. In MDA-MB-468 cells, there was a significant decrease in G0/G1 phases with a substantial increase in the S phase and G2/M phases. In contrast, MDA-MB-231 showed a significant effect only during the two cell cycle stages (S and G2/M), at concentrations of 15 and 20 µM for S phases and all TQ values for G2/M phases. The TQ effect on the apoptotic gene profiles indicated that TQ upregulated 15 apoptotic genes in MDA-MB-231 TNBC cells, including caspases, GADD45A, TP53, DFFA, DIABLO, BNIP3, TRAF2/3, and TNFRSF10A. In MDA-MB-468 cells, 16 apoptotic genes were upregulated, including TNFRSF10A, TNF, TNFRSF11B, FADD TNFRSF10B, CASP2, and TRAF2, all of which are important for the apoptotic pathway andsuppress the expression of one anti-apoptotic gene, BIRC5, in MDA-MB-231 cells. Compared to MDA-MB-231 cells, elevated levels of TNF and their receptor proteins may contribute to their increased sensitivity to TQ-induced apoptosis. It was concluded from this study that TQ targets the MDA-MB-231 and MDA-MB-468 cells differently. Additionally, due to the aggressive nature of TNBC and the lack of specific therapies in chemoresistant TNBC, our findings related to the identified apoptotic gene profile may point to TQ as a potential agent for TNBC therapy.
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Wang, Yun-Hsin, Yau-Hung Chen, and Wen-Hao Shen. "Amikacin Suppresses Human Breast Cancer Cell MDA-MB-231 Migration and Invasion." Toxics 8, no. 4 (November 20, 2020): 108. http://dx.doi.org/10.3390/toxics8040108.
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(1) Background: Amikacin is an aminoglycoside antibiotic used for treating gram-negative bacterial infections in cancer patients. In this study, our aims are to investigate the migratory inhibition effects of amikacin in human MDA-MB-231 cells. (2) Methods: We used a wound-healing assay, trans-well analysis, Western blotting, immunostaining and siRNA knockdown approaches to investigate how amikacin influenced MDA-MB-231 cell migration and invasion. (3) Results: Wound healing showed that the MDA-MB-231 cell migration rates decreased to 44.4% in the presence of amikacin. Trans-well analysis showed that amikacin treatment led to invasion inhibition. Western blotting demonstrated that amikacin induced thioredoxin-interacting protein (TXNIP) up-regulation. TXNIP was knocked down using siRNA in MDA-MB-231 cell. Using immunostaining analysis, we found that inhibition of TXNIP expression led to MDA-MB-231 pseudopodia extension; however, amikacin treatment attenuated the cell extension formation. (4) Conclusions: We observed inhibition of migration and invasion in MDA-MB-231 cells treated with amikacin. This suggests inhibition might be mediated by up-regulation of TXNIP.
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Ayob, Zahidah, Siti Pauliena Mohd Bohari, Azman Abd Samad, and Shajarahtunnur Jamil. "Cytotoxic Activities against Breast Cancer Cells of LocalJusticia gendarussaCrude Extracts." Evidence-Based Complementary and Alternative Medicine 2014 (2014): 1–12. http://dx.doi.org/10.1155/2014/732980.
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Justicia gendarussamethanolic leaf extracts from five different locations in the Southern region of Peninsular Malaysia and two flavonoids, kaempferol and naringenin, were tested for cytotoxic activity. Kaempferol and naringenin were two flavonoids detected in leaf extracts using gas chromatography-flame ionization detection (GC-FID). The results indicated that highest concentrations of kaempferol and naringenin were detected in leaves extracted from Mersing with 1591.80 mg/kg and 444.35 mg/kg, respectively. Positive correlations were observed between kaempferol and naringenin concentrations in all leaf extracts analysed with the Pearson method. The effects of kaempferol and naringenin from leaf extracts were examined on breast cancer cell lines (MDA-MB-231 and MDA-MB-468) using MTT assay. Leaf extract from Mersing showed high cytotoxicity against MDA-MB-468 and MDA-MB-231 with IC50values of 23 μg/mL and 40 μg/mL, respectively, compared to other leaf extracts. Kaempferol possessed high cytotoxicity against MDA-MB-468 and MDA-MB-231 with IC50values of 23 μg/mL and 34 μg/mL, respectively. These findings suggest that the presence of kaempferol in Mersing leaf extract contributed to high cytotoxicity of both MDA-MB-231 and MDA-MB-468 cancer cell lines.
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Maarouf, Rokaya E., Khaled Shaaban Azab, Neama M. El Fatih, Hamed Helal, and Laila Rashed. "Withania somnifera Alter BCL2/Bax signaling and trigger apoptosis of MCF-7 and MDA-MB231 breast cancer cells exposed to γ-radiation." Human & Experimental Toxicology 42 (June 9, 2023): 096032712311808. http://dx.doi.org/10.1177/09603271231180849.
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Treatment strategies encompass synchronization of more than one therapy with specific dependence on zeroing side effects of natural products that might represent a niche in the continuous struggle against cancer. Thus, this study aimed at assessing the role of Withania somnifera; WS (Ashwagandha) in forcing MCF7 or MDA-MB 231 irradiated breast cancer cells to outweigh the route of programmed cell death. We check to what extent SIRT1-BCL2/Bax signaling pathway was interrelated to form apoptotic cancer cells. MDA or MCF7 cells are categorized into four groups: gp1, Control (C): MDA-MB-231 or MCF7 cells not treated with WS or exposed to γ-rays, gp2 (WS): cells challenged with WS for MDA-MB-231 or MCF7 cells respectively, gp3: irradiated (R) MDA-MB-231 or MCF7 cells exposed to γ-rays (4 Gy; one shot) and gp4 WS and irradiated (WS + R): cells challenged with WS as in gp2 and exposed to gamma rays as in gp3. The results revealed that, WS established IC50 equivalent to 4897.8 μg/ml in MDA-MB-231 cells or equivalent to 3801.9 μg/ml in MCF7 cells. The flowcytometric analysis (Annexin V and cell cycle) showed that WS induces apoptosis at pre-G phase and induces cell arrest at G2/M and preG1 phases for MDA-MB-231 and at the preG1 for MCF7 cells. Furthermore, the WS + R group of cells (MDA-MB-231 and MCF7) showed significant increases in the expression of SIRT1, and BCL2 and a decrease in BAX compared with WS or R group. It could be concluded that WS has an anti-proliferative action on MDA-MB-231 and MCF7 cells because of its capability to enhance apoptosis.
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Messeha, Samia S., Najla O. Zarmouh, Lovely Antonie, and Karam F. A. Soliman. "Sanguinarine Inhibition of TNF-α-Induced CCL2, IKBKE/NF-κB/ERK1/2 Signaling Pathway, and Cell Migration in Human Triple-Negative Breast Cancer Cells." International Journal of Molecular Sciences 23, no. 15 (July 28, 2022): 8329. http://dx.doi.org/10.3390/ijms23158329.
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Angiogenesis is a process that drives breast cancer (BC) progression and metastasis, which is linked to the altered inflammatory process, particularly in triple-negative breast cancer (TNBC). In targeting inflammatory angiogenesis, natural compounds are a promising option for managing BC. Thus, this study was designed to determine the natural alkaloid sanguinarine (SANG) potential for its antiangiogenic and antimetastatic properties in triple-negative breast cancer (TNBC) cells. The cytotoxic effect of SANG was examined in MDA-MB-231 and MDA-MB-468 cell models at a low molecular level. In this study, SANG remarkably inhibited the inflammatory mediator chemokine CCL2 in MDA-MB-231 and MDA-MB-468 cells. Furthermore, qRT-PCR confirmed with Western analysis studies showed that mRNA CCL2 repression was concurrent with reducing its main regulator IKBKE and NF-κB signaling pathway proteins in both TNBC cell lines. The total ERK1/2 protein was inhibited in the more responsive MDA-MB-231 cells. SANG exhibited a higher potential to inhibit cell migration in MDA-MB-231 cells compared to MDA-MB-468 cells. Data obtained in this study suggest a unique antiangiogenic and antimetastatic effect of SANG in the MDA-MB-231 cell model. These effects are related to the compound’s ability to inhibit the angiogenic CCL2 and impact the ERK1/2 pathway. Therefore, SANG use may be recommended as a component of the therapeutic strategy for TNBC.
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FLEISHER, BRETT, CAROLIN WERKMAN, BREHANNA JACOBS, JUSTIN VARKEY, KAREEM TAHA, and SIHEM AIT-OUDHIA. "KIFC1: A Reliable Prognostic Biomarker in Rb-positive Triple-negative Breast Cancer Patients Treated With Doxorubicin in Combination With Abemaciclib." Cancer Diagnosis & Prognosis 2, no. 5 (August 30, 2022): 525–32. http://dx.doi.org/10.21873/cdp.10137.
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Background/Aim: Triple-negative breast cancer (TNBC) prevalence and risk of relapse are greatest in African American (AA) patients. Doxorubicin (DOX) and abemaciclib (ABE) synergism in Rb-positive TNBC cells (MDA-MB-231), and antagonism in Rb-negative TNBC cells (MDA-MB-468) have been previously shown. Here, we assessed Kinesin-like protein 1 (KIFC1) as an ethnic-specific prognostic biomarker of the DOX+ABE combination for the Rb-status in TNBC. Materials and Methods: Literature search for TNBC prognostic biomarkers in the AA population was conducted. MDA-MB-231 and MDA-MB-468 cells were exposed over 72 h to four treatment arms: 1) control (medium without drug), 2) DOX at 50% inhibitory concentration in MDA-MB-231 (0.565 μM) and MDA-MB-468 (0.121 μM), 3) ABE alone (2 μM), and 4) DOX+ABE combination at their corresponding concentrations in each cell-line. KIFC1 protein expression and temporal changes were quantified in MDA-MB-231 cells using western blot. Results: KIFC1, Kaiso, and Annexin A2 are literature-identified AA-specific TNBC prognostic biomarkers. KIFC1 was found to be uncorrelated to other proposed biomarkers, suggesting it may predict risk independently of other TNBC biomarkers. In both cell lines, DOX alone did not significantly change KIFC1 expression relative to control. Conversely, ABE reduced KIFC1 expression in MDA-MB-231 but not in MDA-MB-468 cells. The combination DOX+ABE resulted in a greatest reduction in KIFC1 in MDA-MB-231 cells with a more rapid time-to-full inhibition of KIFC1 compared to ABE alone. Conclusion: Change in KIFC1 expression is primarily driven by ABE in Rb-positive TNBC cells. DOX increases ABE speed to achieve a full inhibition of KIFC1 in Rb-positive, yet, without influencing its expression in Rb-negative TNBC cells.
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Chiraatthakit, Benjamas, Benjawan Dunkunthod, Sanong Suksaweang, and Griangsak Eumkeb. "Antiproliferative, Antiangiogenic, and Antimigrastatic Effects of Oroxylum indicum (L.) Kurz Extract on Breast Cancer Cell." Evidence-Based Complementary and Alternative Medicine 2023 (July 8, 2023): 1–13. http://dx.doi.org/10.1155/2023/6602524.
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Breast cancer recurrence continues to pose a major clinical problem, despite significant advancements in early diagnosis and an aggressive mode of treatment. This study aimed at investigating the anticancer activity of Oroxylum indicum extract (OIE) by assessing cell proliferation, cell migration, and angiogenesis in metastatic breast cancer MDA-MB-231 cell lines. This study also estimated the phytochemical profiles of OIE by LC-QTOF-MS. The extract was found to contain six identified flavonoid substances, and baicalein was the most abundant substance in the extract. Cell proliferation capacity was performed by cell counting kit-8 (CCK-8) and colony formation assays. The effect of OIE on cell migration was determined using wound healing and transwell assays. Meanwhile, MDA-MB-231-induced angiogenesis on chick chorioallantoic membrane (CAM) was applied to investigate the ex vivo antiangiogenesis activity of the extracts. OIE at concentrations lower than 600 μg/mL had no cytotoxic effects against MDA-MB-231 cells. OIE was found to inhibit the long-term colony formation ability of MDA-MB-231 cells in a concentration-dependent manner. Antimigration and antiangiogenesis activities were further investigated using noncytotoxic concentrations of OIE ranging from 25 to 150 μg/mL. OIE greatly reduced the migration of MDA-MB-231 breast cancer cells in a dose-dependent manner. OIE significantly suppressed the MDA-MB-231-induced angiogenesis, and there was no substantial toxic effect on natural angiogenesis. Interestingly, the concentration of OIE at 150 μg/mL was as practically potent as pazopanib, the positive anticancer drug, at 4.37 μg/mL in inhibiting MDA-MB-231 cell migration and angiogenesis induced by these cells. Therefore, the inhibitory effects of OIE in cell proliferation and cell migration, together with antiangiogenesis in MDA-MB-231 breast cancer cells, suggesting that OIE has the potential to be a novel adjunct candidate for breast cancer chemotherapeutic agents.
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Song, Tao, and Huazhou Zhang. "RBM8A Depletion Decreases the Cisplatin Resistance and Represses the Proliferation and Metastasis of Breast Cancer Cells via AKT/mTOR Pathway." Breast Journal 2022 (August 28, 2022): 1–13. http://dx.doi.org/10.1155/2022/4576789.
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Background. Breast cancer (BC) is the most prevalent malignancy in women. This study is aimed to explore the role and regulatory mechanism of RNA-binding motif protein 8A (RBM8A) in BC. Methods. We detected the expression of RBM8A in BC tissues and cell lines (MCF-7, MDA-MB-231, and MDA-MB-436), and explored the correlation of RBM8A expression with clinicopathological features in patients. The function of RBM8A deficiency in MCF-7 and MDA-MB-231 cells was determined using MTT, wound healing, and transwell assay. The effect of RBM8A suppression on the cisplatin (DDP) resistance in MCF-7 and MDA-MB-231 cells was also evaluated. Besides, western blotting was used to examine AKT/mTOR pathway-related proteins. The mouse model was constructed to confirm the effect of RBM8A on tumor growth. Results. The expression of RBM8A was elevated in BC tissues and cell lines. RBM8A silencing restrained the malignant behaviors of MCF-7 and MDA-MB-231 cells, including viability, migration, and invasion, while promoting apoptosis. Silencing of RBM8A overcame resistance to DDP in MCF-7 and MDA-MB-231 cells. Furthermore, RBM8A suppression restrained the activation of the AKT/mTOR pathway in both MCF-7 and MDA-MB-231 cells. Feedback experiments revealed that SC79 treatment reversed the reduction effects of RBM8A knockdown on viability, DDP resistance, migration, and invasion of MDA-MB-231 cells. Moreover, the silencing of RBM8A inhibited the growth of tumor xenograft in vivo. Conclusions. RBM8A knockdown may reduce DDP resistance in BC to repress the development of BC via the AKT/mTOR pathway, suggesting that RBM8A may serve as a new therapeutic target in BC.
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Chen, Jung-Chou, Nai-Wen Chang, Jing-Gung Chung, and Kuei-Chu Chen. "Saikosaponin-A Induces Apoptotic Mechanism in Human Breast MDA-MB-231 and MCF-7 Cancer Cells." American Journal of Chinese Medicine 31, no. 03 (January 2003): 363–77. http://dx.doi.org/10.1142/s0192415x03001065.
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The effects of Saikosaponin-A on human breast cancer cell lines (MDA-MB-231 and MCF-7) were investigated. Results demonstrated that Saikosaponin-A inhibited the proliferation or viability of the MDA-MB-231 and MCF-7 cells in a dose-dependent manner. Saikosaponin-A treatment of MDA-MB-231 for 3 hours and of MCF-7 cells for 2 hours, respectively caused an obvious increase in the sub-G1 population of cell cycles. Apoptosis in MDA-MB-231 cells was independent of the P53/p21 pathway mechanism and was accompanied by an increased ratio of Bax to Bcl-2 and c-myc levels and activation of caspase-3. In contrast, apoptosis of MCF-7 cells may have been initiated by the Bcl-2 family of proteins and involved p53/p21 dependent pathway mechanism, and was accompanied by an increased level of c-myc protein. Both the apoptosis of MDA-MB-231 cells and MCF-7 cells showed a difference worthy of further research.
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Ndoye, Abibatou, Rakshitha Pandulal Miskin, and C. Michael DiPersio. "Integrin α3β1 Represses Reelin Expression in Breast Cancer Cells to Promote Invasion." Cancers 13, no. 2 (January 19, 2021): 344. http://dx.doi.org/10.3390/cancers13020344.
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Integrin α3β1, a cell adhesion receptor for certain laminins, is known to promote breast tumor growth and invasion. Our previous gene microarray study showed that the RELN gene, which encodes the extracellular glycoprotein Reelin, was upregulated in α3β1-deficient (i.e., α3 knockdown) MDA-MB-231 cells. In breast cancer, reduced RELN expression is associated with increased invasion and poor prognosis. In this study we demonstrate that α3β1 represses RELN expression to enhance breast cancer cell invasion. RELN mRNA was significantly increased upon RNAi-mediated α3 knockdown in two triple-negative breast cancer cell lines, MDA-MB-231 and SUM159. Modulation of baseline Reelin levels altered invasive potential, where enhanced Reelin expression in MDA-MB-231 cells reduced invasion, while RNAi-mediated suppression of Reelin in SUM159 cells increased invasion. Moreover, treatment of α3β1-expressing MDA-MB-231 cells with culture medium that was conditioned by α3 knockdown MDA-MB-231 cells led to decreased invasion. RNAi-mediated suppression of Reelin in α3 knockdown MDA-MB-231 cells mitigated this effect of conditioned-medium, identifying secreted Reelin as an inhibitor of cell invasion. These results demonstrate a novel role for α3β1 in repressing Reelin in breast cancer cells to promote invasion, supporting this integrin as a potential therapeutic target.
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Liu, H., C. O. Schulz, A. C. Regierer, A. Dieing, K. Possinger, and J. Eucker. "TKI258, a novel, multitargeted tyrosine kinase inhibitor for the treatment of breast cancer." Journal of Clinical Oncology 27, no. 15_suppl (May 20, 2009): e14625-e14625. http://dx.doi.org/10.1200/jco.2009.27.15_suppl.e14625.
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e14625 TKI258 (4-amino-5-fluor-3-[5-(4-metylpiperazin-1-yl)-1H-benzimidazol-2-yl]quinolin-2(1H)-one, formerly known as CHIR258) is an ATP-competitive inhibitor with activities against class III or IV receptor kinases, which include FGFR, VEGFR, PDGFR, FLT3, and KIT. It has been demonstrated to possess strong anti-tumor and anti-angiogenetic activities in different tumor models, and, therefore, this compound is currently being clinically assessed for the treatment of diverse malignancies. In this study, we chose the breast cancer cell line MDA-MB-231, a cell line with high invasive capacities, as an in vitro model to analyze the effect and functional mechanism of TKI258 on the breast cancer invasiveness. Treatment of MDA-MB-231 cells with TKI258 resulted in reduced invasive capacities in a dose-dependent manner. In association with this effect, we observed that TKI258 down-regulated the phosphorylation of ERK1/2 and STAT3 and inhibited the VEGF production in the cell supernatants. Most interestingly, we found TKI258 had influence on the inflammatory chemokines CCL5 and CCL2 level if MDA-MB-231 cells were co-cultured with breast cancer stroma cells. We found that CCL5/CCL2 mRNA level in MDA-MB-231 cells, in stroma cells, or in co-culture of MDA-MB-231/breast cancer stroma was strongly inhibited by TKI258 as detected with real-time PCR. Parallel to this result, the dramatically elevated CCL2/CCL5 level in the media supernatants from co-cultured MDA-MB-231/stroma cells was reduced by TKI258 effectively. Furthermore, we demonstrated that the invasion-promoting effect of the tumor stroma cells was antagonized by TKI258 significantly. CCL5 stimulated invasion of MDA-MB-231 cells could be partially abrogated by TKI58 and/or by CCL5-neutralizing antibody. Therefore, it is most likely that the inhibitory effect of TKI258 on invasion of MDA-MB-231 cells in the presence of stroma cells is achieved, at least in part, by antagonizing the invasion-promoting effect of CCL5. Overall, our data show that TKI258 inhibited invasive capacities of aggressive breast cancer cell line MDA-MB-231, either in the absence or presence of tumor stroma cells in vitro. No significant financial relationships to disclose.
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Yu, Mingming, Yanqin Sun, Guangjie Yang, and Zhenguang Wang. "An Experimental Study on [125I]I-pHLIP (Var7) for SPECT/CT Imaging of an MDA-MB-231 Triple-Negative Breast Cancer Mouse Model by Targeting the Tumor Microenvironment." Molecular Imaging 2021 (February 16, 2021): 1–9. http://dx.doi.org/10.1155/2021/5565932.
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Objective. To evaluate the diagnostic efficacy of MDA-MB-231 triple-negative breast cancer with 125I-labeled pHLIP (Var7) by single-photon emission computed tomography/computed tomography (SPECT/CT) imaging. Methods. The binding fraction of [125I]I-pHLIP (Var7) and MDA-MB-231 cells was measured at pH 7.4 and pH 6.0, and tumor-bearing mice were subjected to small-animal SPECT/CT imaging studies. Results. At pH = 6.0 , the binding fractions of [125I]I-pHLIP (Var7) and MDA-MB-231 cells at 10 min, 40 min, 1 h, and 2 h were 1 .9 ± 0.1 %, 3.5 ± 0.1 %, 6.3 ± 0.8 %, and 6.6 ± 0.3 %, respectively. At pH = 7.4 , there was no measured binding between [125I]I-pHLIP (Var7) and MDA-MB-231 cells. Small-animal SPECT/CT imaging showed clearly visible tumors at 1 and 2 h after injection. Conclusions. [125I]I-pHLIP (Var7) could bind to MDA-MB-231 cells in an acidic environment, and small-animal SPECT/CT imaging showed clear tumors at 1 and 2 h after probe injection.
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Shin, Won-Sik, Si Won Oh, Han Na Park, Jae Hoon Kim, and Seung-Taek Lee. "Knockdown of PTK7 Reduces the Oncogenic Potential of Breast Cancer Cells by Impeding Receptor Tyrosine Kinase Signaling." International Journal of Molecular Sciences 24, no. 15 (July 29, 2023): 12173. http://dx.doi.org/10.3390/ijms241512173.
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Protein tyrosine kinase 7 (PTK7), a catalytically defective receptor tyrosine kinase (RTK), is often upregulated in various cancers. This study aimed to validate PTK7 as a target for breast cancer (BC) and investigate its oncogenic signaling mechanism. BC tissue analysis showed significantly elevated PTK7 mRNA levels, especially in refractory triple-negative breast cancer (TNBC) tissues, compared with normal controls. Similarly, BC cell lines exhibited increased PTK7 expression. Knockdown of PTK7 inhibited the proliferation of T-47D and MCF-7 hormone-receptor-positive BC cell-lines and of HCC1187, MDA-MB-231, MDA-MB-436, and MDA-MB-453 TNBC cells. PTK7 knockdown also inhibited the adhesion, migration, and invasion of MDA-MB-231, MDA-MB-436, and MDA-MB-453 cells, and reduced the phosphorylation levels of crucial oncogenic regulators including extracellular signal-regulated kinase (ERK), Akt, and focal adhesion kinase (FAK). Furthermore, PTK7 interacts with fibroblast growth factor receptor 1 (FGFR1) and epidermal growth factor receptor (EGFR) expressed in MDA-MB-231 cells. Knockdown of PTK7 decreased the growth-factor-induced phosphorylation of FGFR1 and EGFR in MDA-MB-231 cells, indicating its association with RTK activation. In conclusion, PTK7 plays a significant role in oncogenic signal transduction by enhancing FGFR1 and EGFR activation, influencing BC tumorigenesis and metastasis. Hence, PTK7 represents a potential candidate for targeted BC therapy, including TNBC.
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Türköz Uluer, Elgin, Muhammet Yusuf Pekmezci, Hilal Kabadayi Ensarioğlu, and Mahmut Kemal Özbilgin. "Вплив куркуміну та кверцетину на патогенез раку молочної залози шляхом зниження регуляції miR-632 та miR-137." Practical oncology 6, no. 1 (May 9, 2023): 7–12. http://dx.doi.org/10.22141/2663-3272.6.1.2023.78.
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Актуальність. Куркумін і кверцетин виявилися дуже ефективними проти раку молочної залози. Однак повністю їх протипухлинні механізми невідомі. У цьому дослідженні вивчено вплив куркуміну та кверцетину на ріст лінії клітин раку молочної залози людини MCF-7 та MDA-MB-231 шляхом регуляції miR-632 та miR-137. Матеріали та методи. Клітини MCF-7 і MDA-MB-231 обробляли куркуміном і кверцетином у різних розведеннях протягом 24 і 48 годин. Життєздатність клітин оцінювали за допомогою MTT-аналізу. Кількісна полімеразна ланцюгова реакція в реальному часі була використана для виявлення експресії miR-632 і miR-137 у клітинах MCF-7 і MDA-MB-231, оброблених куркуміном і кверцетином. Результати. Наші результати показали, що 50-мкМ розведення куркуміну та кверцетину протягом 24 годин було більш ефективним щодо пригнічення росту клітин MCF-7 та MDA-MB-231. У групах, які отримували куркумін і кверцетин, експресія miR-137 і miR-632 була знижена порівняно з контрольними групами. Експресія miR-137 у клітинній лінії MCF-7 була нижчою, ніж у клітинній лінії MDA-MB-231. Висновки. Використання куркуміну і кверцетину зменшувало ріст лінії клітин раку молочної залози людини MCF-7 і MDA-MB-231 шляхом зниження регуляції miR-137 і miR-632. Цей висновок показав, що куркумін і кверцетин можуть бути використані як терапевтичний засіб, а також що miR-137 і miR-632 застосовуються для діагностики, оцінки ефективності лікування та прогнозу при раку молочної залози.
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Bulut, Derya, Ajda Coker-Gurkan, Recep Genc, Elif Damla Arisan, Pınar Obakan-Yerlikaya, and Narcin Palavan-Unsal. "Autocrine Growth Hormone Mediated Curcumin Resistance Overcame by Autophagy Inhibition via Bafilomycin in MDA-MB-231 and T47D Breast Cancer Cells." Proceedings 2, no. 25 (December 10, 2018): 1569. http://dx.doi.org/10.3390/proceedings2251569.
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Curcumin, a plant derived natural compound, has anti-oxidant, anti-proliferative and apoptotic effect on various cancer cells such as prostate, colon and breast cancer. Autocrine growth hormone (GH) expression induced breast cancer invasion-metastasis has been reported in vivo and in vitro cancer models. Autophagy is a vesicule-mediated clearance mechanism and one of the handicap against drug-induced apoptotic cell death. In this study, our aim was to investigate the molecular machinery of curcumin induced apoptotic cell death under autophagy inhibition conditions in autocrine GH expressing MDA-MB-231 and T47D breast cancer cells. Although autocrine GH induced curcumin resistance, this effect was slightly prevented by time-dependent curcumin treatment in MDA-MB-231 and T47D breast cancer cells. In addition, curcumin induced autophagy vacuole formation was determined by acridine orange staining in MDA-MB-231 and T47D wt/GH+ breast cancer cells. Moreover, curcumin triggered autophagy through upregulating Beclin-1, Atg3, Atg12 expressions and LC3 cleavage in each cell line. Concomitantly, BiP, IRE1α and Calreticulin expressions were upregulated following 3 h curcumin exposure in MDA-MB-231 wt and GH+ cells. According to MTT cell viability assay, autocrine GH-mediated curcumin resistance was overcome by bafilomycin and curcumin co-treatment in MDA-MB-231 and T47D GH+ cells. Moreover, curcumin and bafilomycin co-treatment induced cell cycle arrest at G1 phase in MDA-MB-231 GH+ cells, G2/M arrest in T47D GH+ breast cancer cells. In conclusion, autocrine GH-triggered curcumin resistance was overcome by autophagy inhibition condition by bafilomycin treatment in a dose-dependent manner in MDA-MB-231 and T47D GH+ breast cancer cells.
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Liu, Hengrui, James P. Dilger, and Jun Lin. "Lidocaine Suppresses Viability and Migration of Human Breast Cancer Cells: TRPM7 as a Target for Some Breast Cancer Cell Lines." Cancers 13, no. 2 (January 10, 2021): 234. http://dx.doi.org/10.3390/cancers13020234.
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Background: The local anesthetic lidocaine suppresses some cancer cell lines but the mechanism is unclear. The melastatin-like transient receptor potential 7 (TRPM7) ion channel is aberrantly expressed in some cancers and may play a role in the disease. Hence, we suggested that lidocaine affects the viability and migration of breast cancer cells by regulating TRPM7. Methods: We measured the effects of lidocaine on TRPM7 function in HEK293 with exogenous TRPM7 expression (HEK-M7) using whole-cell patch-clamp and fura-2AM-based quench assay. We measured the effect of lidocaine on TRPM7 function, cell viability, and migration in TRPM7 expressing human breast cancer cell lines using fura-2AM-based quench, MTT, and wound-healing assays respectively. We compared cell viability and migration of wild type HEK293 cells (WT-HEK) with HEK-M7 and wild type MDA-MB-231 (WT-231) with TRPM7 knockout MDA-MB-231 (KO-231). Results: Lidocaine (1–3 mM) inhibited the viability and migration of all of these breast cancer cell lines. Functional evidence for TRPM7 was confirmed in the MDA-MB-231, AU565, T47D, and MDA-MB-468 cell lines where lidocaine at 0.3–3 mM suppressed the TRPM7 function. Lidocaine preferentially suppressed viability and migration of HEK-M7 over WT-HEK and WT-231 over KO-231. Conclusions: Lidocaine differentially reduced the viability and migration of human breast cancer cell lines tested. TRPM7 is one of the potential targets for the effects of lidocaine on viability and migration in MDA-MB-231, AU565, T47D, and MDA-MB-468.
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Liu, Hengrui, James P. Dilger, and Jun Lin. "Lidocaine Suppresses Viability and Migration of Human Breast Cancer Cells: TRPM7 as a Target for Some Breast Cancer Cell Lines." Cancers 13, no. 2 (January 10, 2021): 234. http://dx.doi.org/10.3390/cancers13020234.
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Background: The local anesthetic lidocaine suppresses some cancer cell lines but the mechanism is unclear. The melastatin-like transient receptor potential 7 (TRPM7) ion channel is aberrantly expressed in some cancers and may play a role in the disease. Hence, we suggested that lidocaine affects the viability and migration of breast cancer cells by regulating TRPM7. Methods: We measured the effects of lidocaine on TRPM7 function in HEK293 with exogenous TRPM7 expression (HEK-M7) using whole-cell patch-clamp and fura-2AM-based quench assay. We measured the effect of lidocaine on TRPM7 function, cell viability, and migration in TRPM7 expressing human breast cancer cell lines using fura-2AM-based quench, MTT, and wound-healing assays respectively. We compared cell viability and migration of wild type HEK293 cells (WT-HEK) with HEK-M7 and wild type MDA-MB-231 (WT-231) with TRPM7 knockout MDA-MB-231 (KO-231). Results: Lidocaine (1–3 mM) inhibited the viability and migration of all of these breast cancer cell lines. Functional evidence for TRPM7 was confirmed in the MDA-MB-231, AU565, T47D, and MDA-MB-468 cell lines where lidocaine at 0.3–3 mM suppressed the TRPM7 function. Lidocaine preferentially suppressed viability and migration of HEK-M7 over WT-HEK and WT-231 over KO-231. Conclusions: Lidocaine differentially reduced the viability and migration of human breast cancer cell lines tested. TRPM7 is one of the potential targets for the effects of lidocaine on viability and migration in MDA-MB-231, AU565, T47D, and MDA-MB-468.
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Kong, Yan, Qian Dong, Cuizhi Geng, and Da Jiang. "Effect and mechanism of ikkβ on proliferation, apoptosis, and metastasis of breast cancer cells with different expression levels of leptin and its receptors." Journal of Clinical Oncology 38, no. 15_suppl (May 20, 2020): e15592-e15592. http://dx.doi.org/10.1200/jco.2020.38.15_suppl.e15592.
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e15592 Background: To investigate the effect and mechanism of IKKβ on proliferation, apoptosis, invasion and metastasis of breast cancer cells with different expression levels of leptin and ObR. Methods: IKKβ in breast cancer cells was knocked down via virus transfection technology. MTT, flow cytometry, cell scratch test and clone formation test were used to observe the effect of IKKβ on proliferation, apoptosis and metastasis of breast cancer cells with different expression levels of leptin and ObR. RT-PCR was used to detect the downstream genes expressions in IKKβ signaling pathway. Results: The expression levels of leptin and ObR in MDA-MB-231 cells were higher than those in MCF-7 cells. Lentivirus can successfully infect breast cancer cells in vitro and knock down the expression of IKKβ. Knocking down IKKβ reduced the viability of MDA-MB-231 cells, but had little effect on MCF-7, and had an effect on the cell cycle of both cells. After knocking down IKKβ, the apoptotic rate of MDA-MB-231 cells increased. There was no significant difference in the apoptotic rate of MCF-7 cells. The number of clones of MCF-7 and MDA-MB-231 cells decreased, and the difference was significant. The effect on MDA-MB-231 cells was more significant. The scratch mobility of MDA-MB-231 cells decreased significantly, with significant difference.After knocking down IKKβ, the expressions of leptin and ObR, IKBKG, P65 and HIF in MCF-7 cells were significantly decreased, and there was statistical significance. However, the above indicators were significantly increased in MDA-MB-231 cells. The expression level of IKBKG was increased significantly, whereas that of HIF did not differ significantly, as compared with that of control group. Conclusions: The proliferation, metastasis and apoptosis of MDA-MB-231 cells were inhibited after blocking the IKKβ pathway, while the proliferation of MCF-7 cells was inhibited, and the apoptosis did not change significantly. The difference between the two cells may be related to the different expression levels of leptin and ObR.After blocking the IKKβ signaling pathway, the expressions of genes related to the IKKβ signaling pathway in MDA-MB-231 cells were increased, whereas those in MCF-7 cells were decreased, which might be related to the different expression levels of leptin and ObR.After knocking down IKKβ, the expressions of HIF gene in MCF-7 cells were decreased, whereas those in MDA-MB-231 cell lines were not affected. It needs to be verified whether this difference is related to leptin and ObR.
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Datt, Pulkit, Jinesh Maniar, Prerana P. Dange, Vaishali Kailaje, Mithlesh K. Lakhera, Mansi Samarth, Tanuja Durve, and Sudeep Gupta. "Abstract 78: Microenvironmental cues that regulate breast cancer cellular dormancy in the bone marrow niche." Cancer Research 83, no. 7_Supplement (April 4, 2023): 78. http://dx.doi.org/10.1158/1538-7445.am2023-78.
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Abstract Background: The processes regulating cellular dormancy in tumor cells remain poorly characterized. We investigated the microenvironmental cues responsible for the induction of cellular dormancy in breast cancer cells in different culture scenarios. Methods: We characterized an in vitro model in distinct conditions defined hierarchically by the following: a) normoxia or hypoxia (1% O2 and 5% CO2), b) dishes coated with fibronectin or laminin or none, and c) presence or absence of 10 ng/ml basic fibroblast growth factor (FGF-2) in the culture medium, added on day 0 of culture. Two cell lines (MCF-7 and MDA-MB-231) were cultured at clonogenic densities for 9 days (day-1, day0, up to day+7). The day +7 cells were characterized using crystal violet staining for colony growth (</=12 cells=dormant), p-p38/p-ERK ratio (>1=dormant), Ki67 expression (no expression=dormant) by immunofluorescence, and β-galactosidase staining as a senescence marker. Results: For induction of dormancy in MCF-7 cells, under hypoxic conditions, fibronectin or laminin were sufficient, whereas under normoxic conditions, FGF-2 with fibronectin (but not laminin) was required. For induction of dormancy in MDA-MB-231 cells, under hypoxic conditions, FGF-2 with laminin (but not fibronectin) was sufficient, whereas under normoxic conditions, laminin or fibronectin alone were sufficient, but the addition of FGF-2 led to a proliferative state. The detailed results are shown in Table 1. The dormant cells showed lack of β-galactosidase staining and were viable after 7-day doxorubicin treatment (2 μM), whereas there was complete cell death in proliferating cells. Conclusion: Specific combinations of FGF-2, laminin and fibronectin in microenvironment induce a state of dormancy in MCF-7 and MDA-MB-231 cells under normoxic and hypoxic conditions. The dormant cells show resistance to doxorubicin and lack senescence markers, suggesting their possible role in drug resistance and disease relapse. Table 1. Dormancy induction under specific conditions. Breast cancer cell type Microenvironmental cues p-p38/p-ERK signaling ratio Phenotypic states MDA-MB-231 Normoxia, none (Control) 0.39 Proliferative MDA-MB-231 Normoxia, Fibronectin 1.36 Dormant MDA-MB-231 Normoxia, Laminin 1.69 Dormant MDA-MB-231 Normoxia, FGF-2, Fibronectin 0.21 Proliferative MDA-MB-231 Normoxia, FGF-2, Laminin 0.72 Proliferative MDA-MB-231 Hypoxia, FGF-2, Laminin 1.05 Dormant MDA-MB-231 Hypoxia, FGF-2, Fibronectin 0.26 Proliferative MDA-MB-231 Hypoxia, Laminin 0.27 Proliferative MDA-MB-231 Hypoxia, Fibronectin 0.33 Proliferative MCF-7 Normoxia, none (Control) 1.00 Proliferative MCF-7 Normoxia, FGF-2, Fibronectin 1.44 Dormant MCF-7 Normoxia, FGF-2, Laminin 1.00 Proliferative MCF-7 Normoxia, Fibronectin 0.86 Proliferative MCF-7 Hypoxia, none (Control) 0.93 Proliferative MCF-7 Hypoxia, Fibronectin 2.45 Dormant MCF-7 Hypoxia, Laminin 1.3 Dormant Citation Format: Pulkit Datt, Jinesh Maniar, Prerana P. Dange, Vaishali Kailaje, Mithlesh K. Lakhera, Mansi Samarth, Tanuja Durve, Sudeep Gupta. Microenvironmental cues that regulate breast cancer cellular dormancy in the bone marrow niche [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2023; Part 1 (Regular and Invited Abstracts); 2023 Apr 14-19; Orlando, FL. Philadelphia (PA): AACR; Cancer Res 2023;83(7_Suppl):Abstract nr 78.
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Laukaitienė, Danguolė, Antanas Vaitkus, Aistė Savukaitytė, Roberta Vadeikienė, Arturas Inčiūra, Rasa Ugenskienė, and Elona Juozaitytė. "SKIRTINGŲ KRŪTIES VĖŽIO LĄSTELIŲ LINIJŲ ATSPARUMO RADIOTERAPIJAI TYRIMAS." Health Sciences 31, no. 3 (May 24, 2021): 81–87. http://dx.doi.org/10.35988/sm-hs.2021.085.
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Įvadas. Radioterapija yra vienas iš pagrindinių vėžio gydymo metodų, taikomų daugiau kaip pusei onkologinių pacientų. Manoma, kad pagrindinė onkologinės ligos pasikartojimo ir nesėkmingo gydymo priežastis yra vėžinių ląstelių atsparumas radioterapijai. Viena iš pagrindinių atsparumo radioterapijai priežasčių yra vėžinių ląstelių gebėjimas išvengti apoptozės. Manoma, kad ląstelės ciklas taip pat yra vienas iš procesų, turinčių reikšmės radioatsparumui. Šio tyrimo tikslas – įvertinti skirtingų krūties vėžio ląstelių linijų atsparumą radioterapijai, lyginant jų gyvybingumą, ląstelių pasiskirstymą tarp ciklo fazių ir apoptozės intensyvumą. Metodika. MCF-7 ir MDA-MB-231 ląstelių gyvybingumas buvo ištirtas, naudojant kolonijų formavimo testą. Ląstelės ciklo analizei buvo dažomos propidžio jodidu ir analizuojamos, naudojant tėkmės citometrą Muse Cell Analyzer. Apoptozės intensyvumui nustatyti naudotas aneksinas V ir Guava PCA tėkmės citometras. Rezultatai. Šiame tyrime nustatėme, kad MDA-MB-231 ląstelių gyvybingumas po radioterapijos poveikio buvo didesnis, nei MCF-7 ląstelių. Ciklo analizė parodė, kad po radioterapijos poveikio MCF-7 ląstelių ciklo sustabdymas vyko G0/G1 fazėje, o MDA-MB-231 ląstelių – G2/M fazėje. Po radioterapijos poveikio MCF-7 ląstelėse apoptozė prasidėjo anksčiau ir buvo intensyvesnė, o MDA-MB-231 ląstelės reagavo vėliau ir turėjo uždelstą apoptozinį atsaką. Išvados. MDA-MB-231 ląstelės buvo atsparesnės radioterapijai, negu MCF-7 ląstelės.
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Hosseinpour, Mahnaz, Ahmad Bustamam Abdul, Heshu Sulaiman Rahman, Abdullah Rasedee, Swee Keong Yeap, Negin Ahmadi, Hemn Hassan Othman, and Max Stanley Chartrand. "Comparison of Apoptotic Inducing Effect of Zerumbone and Zerumbone-Loaded Nanostructured Lipid Carrier on Human Mammary Adenocarcinoma MDA-MB-231 Cell Line." Journal of Nanomaterials 2014 (2014): 1–10. http://dx.doi.org/10.1155/2014/742738.
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This study investigated the anticancer effect of zerumbone (ZER) and zerumbone-loaded nanostructured lipid carrier (ZER-NLC) on the human mammary gland adenocarcinoma (MDA-MB-231) cell line. The effect of ZER and ZER-NLC on MDA-MB-231 cells was determined via electron and fluorescent microscopy and flow cytometry using the Annexin V, cell cycle, and Tdt-mediated dUTP nick-end labeling assays. We demonstrated that ZER and ZER-NLC significantly suppressed the proliferation of MDA-MB-231 cells with an IC50of 5.96 ± 0.13 and 6.01 ± 0.11 μg/mL, respectively. ZER and ZER-NLC arrested MDA-MB-231 cell cycle at the G2/M phase. The induction of apoptosis by ZER and ZER-NLC was via the intrinsic pathway through the release of cytochrome c and activation of caspase-3 and caspase-9. The treatments also caused the downregulation of antiapoptotic Bcl-2, Bcl-xL proteins, and proliferating cell nuclear protein and upregulation of proapoptotic Bax protein. Therefore, loading of ZER into NLC did not compromise the anticancer effects of ZER on MDA-MB-231 cells. In conclusion, ZER-NLC, which increased the bioavailability of ZER, is an effective agent in the treatment of cancers.
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Guo, Yubo, and Xiaohua Pei. "Tetrandrine-Induced Autophagy in MDA-MB-231 Triple-Negative Breast Cancer Cell through the Inhibition of PI3K/AKT/mTOR Signaling." Evidence-Based Complementary and Alternative Medicine 2019 (January 1, 2019): 1–11. http://dx.doi.org/10.1155/2019/7517431.
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The present study examined the effects of tetrandrine suppressing proliferation, targeting LC3, p62, and Beclin-1 autophagy genes by inhibiting PI3K/AKT/mTOR signaling in Triple-negative breast cancer (TNBC) MDA-MB-231 cell. Cell viability and apoptosis were evaluated by MTT and Annexin-V/PI double staining. Cytotoxicity was determined with LDH assay. Western Blot and Immunofluorescence were used to measure the protein levels of p62/SQSTM1, Beclin1, LC3-II/LC3-I, and PTEN/PI3K/AKT/mTOR signaling. Results showed that tetrandrine inhibited the MDA-MB-231 cell proliferation and induced the apoptosis. Tetrandrine at doses of 12.8, 16.1, and 25.7μmol/L showed significant cytotoxicity on MDA-MB-231 cells (p<0.01). Tetrandrine induced MDA-MB-231 cell autophagy by decreasing p62/SQSTM1 expression, improving the expression of Beclin1 and LC3-II/LC3-I (p<0.01), inhibiting the PI3K/AKT /mTOR pathway by downregulating the expression of p-AKTser473/AKT, p-PI3K/PI3K p110α, and p-mTORser2448/mTOR and upregulating PTEN expression. These findings revealed that tetrandrine could suppress proliferation and induce autophagy in MDA-MB-231 cell by inhibiting the PI3K/AKT/mTOR pathway and might be a promising anti-triple-negative breast cancer drug.
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Loung, Chao-Yu, Wasundara Fernando, H. P. Vasantha Rupasinghe, and David W. Hoskin. "Apple Peel Flavonoid Fraction 4 Suppresses Breast Cancer Cell Growth by Cytostatic and Cytotoxic Mechanisms." Molecules 24, no. 18 (September 13, 2019): 3335. http://dx.doi.org/10.3390/molecules24183335.
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Many dietary flavonoids possess anti-cancer activities. Here, the effect of apple peel flavonoid fraction 4 (AF4) on the growth of triple-negative (MDA-MB-231, MDA-MB-468), estrogen receptor-positive (MCF-7), and HER2-positive (SKBR3) breast cancer cells was determined and compared with the effect of AF4 on normal mammary epithelial cells and dermal fibroblasts. AF4 inhibited breast cancer cell growth in monolayer cultures, as well as the growth of MCF-7 spheroids, without substantially affecting the viability of non-malignant cells. A sub-cytotoxic concentration of AF4 suppressed the proliferation of MDA-MB-231 cells by inhibiting passage through the G0/G1 phase of the cell cycle. AF4-treated MDA-MB-231 cells also exhibited reduced in vitro migration and invasion, and decreased Akt (protein kinase B) signaling. Higher concentrations of AF4 were selectively cytotoxic for MDA-MB-231 cells. AF4 cytotoxicity was associated with the intracellular accumulation of reactive oxygen species. Importantly, intratumoral administration of AF4 suppressed the growth of MDA-MB-231 xenografts in non-obese diabetic severe combined immunodeficient (NOD-SCID) female mice. The selective cytotoxicity of AF4 for breast cancer cells, combined with the capacity of sub-cytotoxic AF4 to inhibit breast cancer cell proliferation, migration, and invasion suggests that flavonoid-rich AF4 (and its constituents) has potential as a natural therapeutic agent for breast cancer treatment.
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Cantonero, Carlos, Pedro Javier Camello, Carmen Abate, Francesco Berardi, Gines Maria Salido, Juan Antonio Rosado, and Pedro C. Redondo. "NO1, a New Sigma 2 Receptor/TMEM97 Fluorescent Ligand, Downregulates SOCE and Promotes Apoptosis in the Triple Negative Breast Cancer Cell Lines." Cancers 12, no. 2 (January 21, 2020): 257. http://dx.doi.org/10.3390/cancers12020257.
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(1) Background: The structure of the Sigma 2 receptor/TMEM97 (σ2RTMEM97) has recently been reported. (2, 3) Methods and results: We used genetic and biochemical approaches to identify the molecular mechanism downstream of σ2R/TMEM97. The novel σ2R/TMEM97 fluorescent ligand, NO1, reduced the proliferation and survival of the triple negative breast cancer cell lines (TNBC: MDA-MB-231 and MDA-MB-468 cell lines), due to NO1-induced apoptosis. Greater bioaccumulation and faster uptake of NO1 in MDA-MB-231 cells compared to MCF10A or MCF7 cell lines were also shown. Accordingly, elevated σ2R/TMEM97 expression was confirmed by Western blotting. In contrast to NO1, other σ2R/TMEM97 ligands, such as SM21 and PB28, enhanced MDA-MB-231 cell proliferation and migration. Store-operated calcium entry (SOCE) is crucial for different cancer hallmarks. Here, we show that NO1, but not other σ2R/TMEM97 ligands, reduced SOCE in MDA-MB-231 cells. Similarly, TMEM97 silencing in MDA-MB-231 cells also impaired SOCE. NO1 administration downregulated STIM1-Orai1 interaction, probably by impairing the positive regulatory effect of σ2R/TMEM97 on STIM1, as we were unable to detect interaction with Orai1. (4) Conclusion: σ2R/TMEM97 is a key protein for the survival of triple negative breast cancer cells by promoting SOCE; therefore, NO1 may become a good pharmacological tool to avoid their proliferation.
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Velmurugan, Bharath Kumar, Po-Chih Wang, and Ching-Feng Weng. "16-Hydroxycleroda-3,13-dien-15,16-olide and N-Methyl-Actinodaphine Potentiate Tamoxifen-Induced Cell Death in Breast Cancer." Molecules 23, no. 8 (August 6, 2018): 1966. http://dx.doi.org/10.3390/molecules23081966.
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In this study, we investigated whether 16-hydroxycleroda-3,13-dien-15,16-olide (HCD) and N-methyl-actinodaphine (MA) could sensitize breast cancer cells to Tamoxifen (TMX) treatment. MA or HCD alone or in combination with TMX dose-dependently inhibited MCF-7 and MDA-MB-231 cell growth, with a more potent inhibition on MDA-MB 231 cells. Furthermore, this novel combination significantly induced S and G2/M cell cycle phase in MDA-MB 231 than MCF-7 cells. Further determination of the apoptotic induction showed that MA or HCD and TMX combination inhibited MDA-MB-231 and MCF-7 cancer cells by upregulating Bax and by downregulating Bcl-2 mRNA and protein expression without altering Caspase-8 and Caspase-12 expression. These results suggest that MA or HCD pretreatment may potentiate the anti-tumor effect of tamoxifen on breast cancer.
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López, Jose J., Geraldine Siegfried, Carlos Cantonero, Fabienne Soulet, Jean Descarpentrie, Tarik Smani, Iker Badiola, et al. "Furin Prodomain ppFurin Enhances Ca2+ Entry Through Orai and TRPC6 Channels’ Activation in Breast Cancer Cells." Cancers 13, no. 7 (April 1, 2021): 1670. http://dx.doi.org/10.3390/cancers13071670.
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The intracellular calcium concentration ([Ca2+]i) modulation plays a key role in the regulation of cellular growth and survival in normal cells and failure of [Ca2+]i homeostasis is involved in tumor initiation and progression. Here we showed that inhibition of Furin by its naturally occurring inhibitor the prodomain ppFurin in the MDA-MB-231 breast cancer cells resulted in enhanced store-operated calcium entry (SOCE) and reduced the cell malignant phenotype. Expression of ppFurin in a stable manner in MDA-MB-231 and the melanoma MDA-MB-435 cell lines inhibits Furin activity as assessed by in vitro digestion assays. Accordingly, cell transfection experiments revealed that the ppFurin-expressing cells are unable to adequately process the proprotein convertase (PC) substrates vascular endothelial growth factor C (proVEGF-C) and insulin-like growth factor-1 receptor (proIGF-1R). Compared to MDA-MB-435 cells, expression of ppFurin in MDA-MB-231 and BT20 cells significantly enhanced SOCE and induced constitutive Ca2+ entry. The enhanced SOCE is impaired by inhibition of Orai channels while the constitutive Ca2+ entry is attenuated by silencing or inhibition of TRPC6 or inhibition of Orai channels. Analysis of TRPC6 activation revealed its upregulated tyrosine phosphorylation in ppFurin-expressing MDA-MB-231 cells. In addition, while ppFurin had no effect on MDA-MB-435 cell viability, in MDA-MB-231 cells ppFurin expression reduced their viability and ability to migrate and enhanced their sensitization to the apoptosis inducer hydrogen peroxide and similar results were observed in BT20 cells. These findings suggest that Furin inhibition by ppFurin may be a useful strategy to interfere with Ca2+ mobilization, leading to breast cancer cells’ malignant phenotype repression and reduction of their resistance to treatments.
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Gaule, Patricia, Nupur Mukherjee, Brendan Corkery, Alex Eustace, Kathy Gately, Sandra Roche, Robert O’Connor, et al. "Dasatinib Treatment Increases Sensitivity to c-Met Inhibition in Triple-Negative Breast Cancer Cells." Cancers 11, no. 4 (April 17, 2019): 548. http://dx.doi.org/10.3390/cancers11040548.
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In pre-clinical studies, triple-negative breast cancer (TNBC) cells have demonstrated sensitivity to the multi-targeted kinase inhibitor dasatinib; however, clinical trials with single-agent dasatinib showed limited efficacy in unselected populations of breast cancer, including TNBC. To study potential mechanisms of resistance to dasatinib in TNBC, we established a cell line model of acquired dasatinib resistance (231-DasB). Following an approximately three-month exposure to incrementally increasing concentrations of dasatinib (200 nM to 500 nM) dasatinib, 231-DasB cells were resistant to the agent with a dasatinib IC50 value greater than 5 μM compared to 0.04 ± 0.001 µM in the parental MDA-MB-231 cells. 231-DasB cells also showed resistance (2.2-fold) to the Src kinase inhibitor PD180970. Treatment of 231-DasB cells with dasatinib did not inhibit phosphorylation of Src kinase. The 231-DasB cells also had significantly increased levels of p-Met compared to the parental MDA-MB-231 cells, as measured by luminex, and resistant cells demonstrated a significant increase in sensitivity to the c-Met inhibitor, CpdA, with an IC50 value of 1.4 ± 0.5 µM compared to an IC50 of 6.8 ± 0.2 µM in the parental MDA-MB-231 cells. Treatment with CpdA decreased p-Met and p-Src in both 231-DasB and MDA-MB-231 cells. Combined treatment with dasatinib and CpdA significantly inhibited the growth of MDA-MB-231 parental cells and prevented the emergence of dasatinib resistance. If these in vitro findings can be extrapolated to human cancer treatment, combined treatment with dasatinib and a c-Met inhibitor may block the development of acquired resistance and improve response rates to dasatinib treatment in TNBC.
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Uçar, Meltem, and Orhan Değer. "Morphological evaluation of MDA-MB-231 human breast cancer cells treated with DMEM extract of Turkish propolis." Tropical Journal of Pharmaceutical Research 18, no. 5 (May 25, 2021): 935–39. http://dx.doi.org/10.4314/tjpr.v18i5.4.
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Purpose: To evaluate the influence of DMEM extract of Turkish propolis (TP) on the morphology of metastatic MDA-MB-231 cells.
Methods: The cells were incubated with DMEM extract of TP (collected from Trabzon in Turkey) at a dose of 2.5 mg/mL for 72 h. The effect of DMEM extract on proliferation and cytotoxicity of the cells was determined using 3-[4,5-dimethyltiazol-2-yl]-2,5-diphenyltetrazolium bromide (MTT) and trypan blue exclusion assay. MDA-MB-231 cells incubated with or without extracts were randomly photographed with a camera-coupled inverted microscope. Treated and control MDA-MB-231 cells were classified as monopolar, bipolar or multipolar, and their dimensions measured with an electronic caliper.
Results: Although the extract reduced the proliferation of the cells, the effect was not statistically significant (p < 0.05). Moreover, no cytotoxic effect was observed. Field diameters, process length and cell body diameters of the treated cells were increased by DMEM extract treatment in bipolar and multipolar cell types, but these parameters were decreased in monopolar cell type, although insignificantly (p < 0.05). In addition, the process thickness of treated MDA-MB-231 cells increased insignificantly in all cell types (p < 0.05).
Conclusion: These findings indicate that DMEM extract of TP at a dose of 2.5 mg/mL morphologically suppresses monopolar MDA-MB-231 cells. Future studies would examine the morphological effects of different concentrations of the propolis extract in anti-proliferation, cytotoxicity and morphological investigations in MDA-MB-231 cells.
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Nguyen, Yen Thi-Kim, Jeong Yong Moon, Meran Keshawa Ediriweera, and Somi Kim Cho. "Phenethyl Isothiocyanate Suppresses Stemness in the Chemo- and Radio-Resistant Triple-Negative Breast Cancer Cell Line MDA-MB-231/IR Via Downregulation of Metadherin." Cancers 12, no. 2 (January 22, 2020): 268. http://dx.doi.org/10.3390/cancers12020268.
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Resistance to chemotherapy and radiation therapy is considered a major therapeutic barrier in breast cancer. Cancer stem cells (CSCs) play a prominent role in chemo and radiotherapy resistance. The established chemo and radio-resistant triple-negative breast cancer (TNBC) cell line MDA-MB-231/IR displays greater CSC characteristics than the parental MDA-MB-231 cells. Escalating evidence demonstrates that metadherin (MTDH) is associated with a number of cancer signaling pathways as well as breast cancer therapy resistance, making it an attractive therapeutic target. Kaplan–Meier plot analysis revealed a correlation between higher levels of MTDH and shorter lifetimes in breast cancer and TNBC patients. Moreover, there was a positive correlation between the MTDH and CD44 expression levels in The Cancer Genome Atlas breast cancer database. We demonstrate that MTDH plays a pivotal role in the regulation of stemness in MDA-MB-231/IR cells. Knockdown of MTDH in MDA-MB-231/IR cells resulted in a reduction in the CSC population, aldehyde dehydrogenase activity, and major CSC markers, including β-catenin, CD44+, and Slug. In addition, MTDH knockdown increased reactive oxygen species (ROS) levels in MDA-MB-231/IR cells. We found that phenethyl isothiocyanate (PEITC), a well-known pro-oxidant phytochemical, suppressed stemness in MDA-MB-231/IR cells through ROS modulation via the downregulation of MTDH. Co-treatment of PEITC and N-Acetylcysteine (a ROS scavenger) caused alterations in PEITC induced cell death and CSC markers. Moreover, PEITC regulated MTDH expression at the post-transcriptional level, which was confirmed using cycloheximide, a protein synthesis inhibitor.
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Jang, Hye-Yeon, Song-Hee Lee, In-Jung An, Hae-Nim Lee, Hye-Ri Kim, Young-Seok Park, Byung-Kwon Park, et al. "Effects of Delphinidin in Anthocyanin on MDA-MB-231 Breast Cancer Cells." Journal of the Korean Society of Food Science and Nutrition 43, no. 2 (February 28, 2014): 231–37. http://dx.doi.org/10.3746/jkfn.2014.43.2.231.
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Risha, Yousef, Vanessa Susevski, Nico Hüttmann, Suttinee Poolsup, Zoran Minic, and Maxim V. Berezovski. "Breast Cancer-Derived Microvesicles Are the Source of Functional Metabolic Enzymes as Potential Targets for Cancer Therapy." Biomedicines 9, no. 2 (January 22, 2021): 107. http://dx.doi.org/10.3390/biomedicines9020107.
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Membrane-derived extracellular vesicles, referred to as microvesicles (MVs), have been proposed to participate in several cancer diseases. In this study, MV fractions were isolated by differential ultracentrifugation from a metastatic breast cancer (BC) cell line MDA-MB-231 and a non-cancerous breast cell line MCF10A, then analyzed by nano-liquid chromatography coupled to tandem mass spectrometry. A total of 1519 MV proteins were identified from both cell lines. The data obtained were compared to previously analyzed proteins from small extracellular vesicles (sEVs), revealing 1272 proteins present in both MVs and sEVs derived from the MDA-MB-231 cell line. Among the 89 proteins unique to MDA-MB-231 MVs, three enzymes: ornithine aminotransferase (OAT), transaldolase (TALDO1) and bleomycin hydrolase (BLMH) were previously proposed as cancer therapy targets. These proteins were enzymatically validated in cells, sEVs, and MVs derived from both cell lines. The specific activity of OAT and TALDO1 was significantly higher in MDA-MB-231-derived MVs than in MCF10A MVs. BLMH was highly expressed in MDA-MB-231-derived MVs, compared to MCF10A MVs. This study shows that MVs carry functional metabolic enzymes and provides a framework for future studies of their biological role in BC and potential in therapeutic applications.
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Qi, Zhaozhen, Shuangxi Kong, Shunyu Zhao, and Qiu Tang. "Naringenin inhibits human breast cancer cells (MDA-MB-231) by inducing programmed cell death, caspase stimulation, G2/M phase cell cycle arrest and suppresses cancer metastasis." Cellular and Molecular Biology 67, no. 2 (September 29, 2021): 8–13. http://dx.doi.org/10.14715/cmb/2021.67.2.2.
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The current study was designed to unveil the anticancer effects of naringenin against breast cancer MDA-MB-231 cells. Cytotoxic effects were estimated via MTT viability assay. Clonogenic assay was performed to assess clonogenic potential of MDA-MB-231 cells. Apoptosis was examined via AO/EB staining, quantified via annexin V/PI staining and western blotting was performed to monitor apoptosis allied protein expressions. Cell cycle was analyzed through flow cytometric analysis. Transwell chambers assay was executed for determination of cell migration and cell invasion tendency of MDA-MB-231 breast cancer cells. Results indicated significant anticancer potential of naringenin drug against MDA-MB-231 cells. On evaluation of cell proliferation rate of breast cancer cells by MTT assay, it was observed that naringenin inhibited proliferation rate in dose as well as time dependent manner. AO/EB staining assay revealed potential morphological changes indicating apoptotic cell death. Annexin V/PI staining assay revealed increased apoptotic cell percentage with increased drug doses. The apoptosis inducing potential of naringenin drug was observed to be mediated via caspase activation. Flow cytometric analysis predicted cell cycle arrest at G2/M phase of cell cycle. Further cell migration as well as cell invasion tendency of MDA-MB-231 cells was reduced to minimum upon application of naringenin drug.
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Zemljič-Jokhadar, Špela, Gašper Kokot, Mojca Pavlin, and Jure Derganc. "Adhesion and Stiffness of Detached Breast Cancer Cells In Vitro: Co-Treatment with Metformin and 2-Deoxy-d-glucose Induces Changes Related to Increased Metastatic Potential." Biology 10, no. 9 (September 4, 2021): 873. http://dx.doi.org/10.3390/biology10090873.
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Metastatic cancer cells can overcome detachment-induced cell death and can proliferate in anchorage-independent conditions. A recent study revealed that a co-treatment with two drugs that interfere with cell metabolism, metformin and 2-deoxy-D-glucose, promotes detachment of viable MDA-MB-231 breast cancer cells. In the present study, we analyzed if these detached viable MDA-MB-231 cells also exhibit other features related to cancer metastatic potential, i.e., if they are softer and more prone to adhere to epithelial cells. The cell mechanics of attached cells and floating cells were analyzed by optical tweezers and cell deformability cytometry, respectively. The adhesion was assessed on a confluent monolayer of HUVEC cells, with MDA-MB-231 cells either in static conditions or in a microfluidic flow. Additionally, to test if adhesion was affected by the state of the epithelial glycocalyx, HUVEC cells were treated with neuraminidase and tunicamycin. It was found that the treated MDA-MB-231 cells were more prone to adhere to HUVEC cells and that they were softer than the control, both in the floating state and after re-seeding to a substrate. The changes in the HUVEC glycocalyx, however, did not increase the adhesion potential of MDA-MB-231.
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Handayani, Sri, Ratna Asmah Susidarti, Puspa Dewi Narrij Lotulung, Akhmad Darmawan, Edy Meiyanto, and Riris Istighfari Jenie. "Antimigratory Activity of Brazilin-Containing Fraction from Caesalpinia sappan L. on MDAMB-231 Cells." HAYATI Journal of Biosciences 27, no. 4 (October 1, 2020): 266. http://dx.doi.org/10.4308/hjb.27.4.266.
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Caesalpinia sappan is studied for several biological activities. The aim of this research is to determine the cytotoxic and antimigratory activities of Caesalpinia sappan active fraction in combination with cisplatin on human TNBC cells (MDA-MB-231). Caesalpinia sappan heartwood was extracted with methanol. Then, several fractions of the methanol extract were obtained by using a liquid-liquid extraction method followed by column chromatography. The cytotoxicity was determined using MTT assay. Synergistic effects were analyzed by calculating the combination index (CI). Migration was examined using wound-healing assay. Levels of MMP2 activity were determined with gelatin zymography assay. The results showed that most of the fractions included in this study exhibited cytotoxic effects against MDA-MB-231 cells, and C fraction demonstrated the highest cytotoxic activity of all fractions. The combination of C-cisplatin revealed a synergistic inhibitory effect on MDA-MB-231 cell growth (CI<1). Furthermore, C fraction, alone and in combination with cisplatin, inhibited migration of MDA-MB-231 and suppressed MMP2 activity. The C fraction isolated from Caesalpinia sappan increased the cytotoxic and antimigratory activities of cisplatin on MDA-MB-231 cells. Based on these findings, the potential of Caesalpinia sappan to act as a supportive agent in metastatic TNBC treatment with cisplatin warrants further exploration.
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Ma, Bin, Wenjia Guo, Meihui Shan, Nan Zhang, Binlin Ma, and Gang Sun. "BRCA1 subcellular localization regulated by PI3K signaling pathway in triple-negative breast cancer MDA-MB-231 cells and hormone-sensitive T47D cells." Open Life Sciences 15, no. 1 (July 10, 2020): 501–10. http://dx.doi.org/10.1515/biol-2020-0054.
Full textAbstract:
AbstractThis study is to investigate the effect of the PI3K/Akt signaling pathway on the regulation of BRCA1 subcellular localization in triple-negative breast cancer (TNBC) MDA-MB-231 cells and hormone-sensitive T47D cells. We found that heregulin-activated T47D cells showed more nuclear localization of BRCA1, but BRCA1 nuclear localization decreased after the inhibition of the PI3K signaling pathway. In MDA-MB-231 cells, activation or inhibition of the PI3K signaling pathway did not significantly affect cell apoptosis and BRCA1 nuclear translocation (P > 0.05). However, in T47D cells, the activation of the PI3K pathway significantly increased cell apoptosis (P < 0.05). In the heregulin-activated MDA-MB-231 and T47D cells, the phosphorylation of Akt and BRCA1 was significantly increased (P < 0.05), while that was significantly reduced after PI3K pathway inhibition (P < 0.05). The changing trends of the mRNA levels of Akt and BRCA1 in MDA-MB-231 and T47D cells after PI3K pathway activation or inhibition were consistent with the trends of their proteins. In both MDA-MB-231 and T47D cells, BRCA1 phosphorylation is regulated by the PI3K signaling pathway, but the nuclear localization of BRCA1 is different in these two cell lines. Moreover, the apoptosis rates of these two cell lines are different.
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Li, Qi, Zehui Gu, Qi Tan, Liqun Ren, and Suxian Chen. "MicroRNA-129-1-3p Represses the Progression of Triple-Negative Breast Cancer by Targeting the GRIN2D Gene." BioMed Research International 2022 (March 7, 2022): 1–9. http://dx.doi.org/10.1155/2022/1549357.
Full textAbstract:
The aberrant expression of miRNA is strongly linked to numerous stages of triple-negative breast cancer (TNBC) progression, and it plays an indispensable role in the process from tumor onset and progress to invasion and metastasis. In this study, we first transfected miR-129-1-3p mimics and inhibitor into MDA-MB-231 TNBC cells, respectively. Then, we assessed the pathological role of miR-129-1-3p in MDA-MB-231 cells. The results showed that miR-129-1-3p were successfully inserted into MDA-MB-231 cells. Besides, miR-129-1-3p could distinctively repress the growth, migration along with infiltration of MDA-MB-231 cells, which might be related to the inhibition of GRIN2D expression. Our results indicate that miR-129-1-3p was illustrated to serve as a tumor repressor via targeting GRIN2D in TNBC cells and highlight that the restoration of miR-129-1-3p might be a new treatment target for TNBC.
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Adinew, Getinet M., Samia Messeha, Equar Taka, Bereket Mochona, Kinfe K. Redda, and Karam F. A. Soliman. "Thymoquinone Inhibition of Chemokines in TNF-α-Induced Inflammatory and Metastatic Effects in Triple-Negative Breast Cancer Cells." International Journal of Molecular Sciences 24, no. 12 (June 8, 2023): 9878. http://dx.doi.org/10.3390/ijms24129878.
Full textAbstract:
The lack of identifiable molecular targets or biomarkers hinders the development of treatment options in triple-negative breast cancer (TNBC). However, natural products offer a promising alternative by targeting inflammatory chemokines in the tumor microenvironment (TME). Chemokines are crucial in promoting breast cancer growth and metastasis and correlate to the altered inflammatory process. In the present study, we evaluated the anti-inflammatory and antimetastatic effects of the natural product thymoquinone (TQ) on TNF-α-stimulated TNBC cells (MDA-MB-231 and MDA-MB-468) to study the cytotoxic, antiproliferative, anticolony, antimigratory, and antichemokine effects using enzyme-linked immunosorbent assays, quantitative real-time reverse transcription–polymerase chain reactions, and Western blots were used in sequence to validate the microarray results further. Four downregulated inflammatory cytokines were identified, CCL2 and CCL20 in MDA-MB-468 cells and CCL3 and CCL4 in MDA-MB-231 cells. Furthermore, when TNF-α-stimulated MDA-MB-231 cells were compared with MDA-MB-468 cells, the two cells were sensitive to TQ’s antichemokine and antimetastatic effect in preventing cell migration. It was concluded from this investigation that genetically different cell lines may respond to TQ differently, as TQ targets CCL3 and CCL4 in MDA-MB-231 cells and CCL2 and CCL20 in MDA-MB-468 cells. Therefore, the results indicate that TQ may be recommended as a component of the therapeutic strategy for TNBC treatment. These outcomes stem from the compound’s capacity to suppress the chemokine. Even though these findings support the usage of TQ as part of a therapy strategy for TNBC associated with the identified chemokine dysregulations, additional in vivo studies are needed to confirm these in vitro results.