Thematische Bibliographien / MDA-MB-231

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  2. Dissertationen
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Auswahl der wissenschaftlichen Literatur zum Thema „MDA-MB-231“

Autor: Grafiati
Veröffentlicht am 4. Juni 2021
Zuletzt aktualisiert am 6. September 2023

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Zeitschriftenartikel zum Thema "MDA-MB-231"

1

Paramanantham, Anjugam, Eun Joo Jung, Se-IL Go, Bae Kwon Jeong, Jin-Myung Jung, Soon Chan Hong, Gon Sup Kim und 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, Nr. 9 (06.05.2021): 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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2

Jin, Hana, Young Shin Ko, Sang Won Park, Ki Churl Chang und Hye Jung Kim. „13-Ethylberberine Induces Apoptosis through the Mitochondria-Related Apoptotic Pathway in Radiotherapy-Resistant Breast Cancer Cells“. Molecules 24, Nr. 13 (04.07.2019): 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.
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3

Yuan, Fahu, Xinghua Liao und 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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4

Ko, Young Shin, Trojan Rugira, Hana Jin, Young Nak Joo und 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, Nr. 21 (28.10.2020): 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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5

Yang, Ji, Yue Wu, Xiao Wang, Liqian Xu, Xiaohong Zhao und Yunmei Yang. „Chemoresistance is associated with overexpression of HAX-1, inhibition of which resensitizes drug-resistant breast cancer cells to chemotherapy“. Tumor Biology 39, Nr. 3 (März 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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6

Risha, Y., V. Susevski, N. Hüttmann, S. Poolsup, Z. Minic und M. V. Berezovski. „Proteome of breast cancer derived microvesicles“. Siberian Medical Review, Nr. 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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7

Trieu, V., S. Ran, C. Bivens und N. Desai. „Chemoprotection by VEGF: Rationale for combination nab-paclitaxel and bevacizumab“. Journal of Clinical Oncology 25, Nr. 18_suppl (20.06.2007): 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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8

Lee, Hwan Hee, Joohee Jung, Aree Moon, Hyojeung Kang und 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, Nr. 13 (27.06.2019): 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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9

Alva, A. S., Z. Varsos, H. Roca und K. Pienta. „Effect of CCL2 on survival of breast cancer MDA-MB-231 cells via inhibition of apoptosis“. Journal of Clinical Oncology 27, Nr. 15_suppl (20.05.2009): 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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10

Jin, Hana, Trojan Rugira, Young Shin Ko, Sang Won Park, Seung Pil Yun und Hye Jung Kim. „ESM-1 Overexpression is Involved in Increased Tumorigenesis of Radiotherapy-Resistant Breast Cancer Cells“. Cancers 12, Nr. 6 (26.05.2020): 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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Dissertationen zum Thema "MDA-MB-231"

1

Esmaeili, Pourfarhangi Kamyar. „Movie8: FUCCI-MDA-MB-231 cells migration on 2D gelatin“. Diss., Cancer Invasion; Cell Migration; Chemotaxis; Contact Guidance; Invadopodia; Mechanobiology, 2019. http://cdm16002.contentdm.oclc.org/cdm/ref/collection/p245801coll10/id/584750.

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Bioengineering;
Ph.D.;
Metastasis is the leading cause of death among cancer patients. The metastatic cascade, during which cancer cells from the primary tumor reach a distant organ and form multiple secondary tumors, consists of a series of events starting with cancer cells invasion through the surrounding tissue of the primary tumor. Invading cells may perform proteolytic degradation of the surrounding extracellular matrix (ECM) and directed migration in order to disseminate through the tissue. Both of the mentioned processes are profoundly affected by several parameters originating from the tumor microenvironment (extrinsic) and tumor cells themselves (intrinsic). However, due to the complexity of the invasion process and heterogeneity of the tumor tissue, the exact effect of many of these parameters are yet to be elucidated. ECM proteolysis is widely performed by cancer cells to facilitate the invasion process through the dense and highly cross-linked tumor tissue. It has been shown in vivo that the proteolytic activity of the cancer cells correlates with the cross-linking level of their surrounding ECM. Therefore, the first part of this thesis seeks to understand how ECM cross-linking regulates cancer cells proteolytic activity. This chapter first quantitatively characterizes the correlation between ECM cross-linking and the dynamics of cancer cells proteolytic activity and then identifies ß1-integrin subunit as a master regulator of this process. Once cancer cells degrade their immediate ECM, they directionally migrate through it. Bundles of aligned collagen fibers and gradients of soluble growth factors are two well-known cues of directed migration that are abundantly present in tumor tissues stimulating contact guidance and chemotaxis, respectively. While such cues direct the cells towards a specific direction, they are also known to stimulate cell cycle progression. Moreover, due to the complexity of the tumor tissue, cells may be exposed to both cues simultaneously, and this co-stimulation may happen in the same or different directions. Hence, in the next two chapters of this thesis, the effect of cell cycle progression and contact guidance-chemotaxis dual-cue environments on directional migration of invading cells are assessed. First, we show that cell cycle progression affects contact guidance and not random motility of the cells. Next, we show how exposure of cancer cells to contact guidance-chemotaxis dual-cue environments can improve distinctive aspects of cancer invasion depending on the spatial conformation of the two cues. In this dissertation, we strive to achieve the defined milestones by developing novel mathematical and experimental models of cancer invasion as well as utilizing fluorescent time-lapse microscopy and automated image and signal processing techniques. The results of this study improve our knowledge about the role of the studied extrinsic and intrinsic cues in cancer invasion.
Temple University--Theses
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2

Esmaeili, Pourfarhangi Kamyar. „Movie9: FUCCI-MDA-MB-231 cells migration inside the microchannels“. Diss., Cancer Invasion; Cell Migration; Chemotaxis; Contact Guidance; Invadopodia; Mechanobiology, 2019. http://cdm16002.contentdm.oclc.org/cdm/ref/collection/p245801coll10/id/584759.

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Bioengineering;
Ph.D.;
Metastasis is the leading cause of death among cancer patients. The metastatic cascade, during which cancer cells from the primary tumor reach a distant organ and form multiple secondary tumors, consists of a series of events starting with cancer cells invasion through the surrounding tissue of the primary tumor. Invading cells may perform proteolytic degradation of the surrounding extracellular matrix (ECM) and directed migration in order to disseminate through the tissue. Both of the mentioned processes are profoundly affected by several parameters originating from the tumor microenvironment (extrinsic) and tumor cells themselves (intrinsic). However, due to the complexity of the invasion process and heterogeneity of the tumor tissue, the exact effect of many of these parameters are yet to be elucidated. ECM proteolysis is widely performed by cancer cells to facilitate the invasion process through the dense and highly cross-linked tumor tissue. It has been shown in vivo that the proteolytic activity of the cancer cells correlates with the cross-linking level of their surrounding ECM. Therefore, the first part of this thesis seeks to understand how ECM cross-linking regulates cancer cells proteolytic activity. This chapter first quantitatively characterizes the correlation between ECM cross-linking and the dynamics of cancer cells proteolytic activity and then identifies ß1-integrin subunit as a master regulator of this process. Once cancer cells degrade their immediate ECM, they directionally migrate through it. Bundles of aligned collagen fibers and gradients of soluble growth factors are two well-known cues of directed migration that are abundantly present in tumor tissues stimulating contact guidance and chemotaxis, respectively. While such cues direct the cells towards a specific direction, they are also known to stimulate cell cycle progression. Moreover, due to the complexity of the tumor tissue, cells may be exposed to both cues simultaneously, and this co-stimulation may happen in the same or different directions. Hence, in the next two chapters of this thesis, the effect of cell cycle progression and contact guidance-chemotaxis dual-cue environments on directional migration of invading cells are assessed. First, we show that cell cycle progression affects contact guidance and not random motility of the cells. Next, we show how exposure of cancer cells to contact guidance-chemotaxis dual-cue environments can improve distinctive aspects of cancer invasion depending on the spatial conformation of the two cues. In this dissertation, we strive to achieve the defined milestones by developing novel mathematical and experimental models of cancer invasion as well as utilizing fluorescent time-lapse microscopy and automated image and signal processing techniques. The results of this study improve our knowledge about the role of the studied extrinsic and intrinsic cues in cancer invasion.
Temple University--Theses
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3

Esmaeili, Pourfarhangi Kamyar. „Movie2: MDA-MB-231 cell switching between Migration and Invadopodia states“. Diss., Temple University Libraries, 2019. http://cdm16002.contentdm.oclc.org/cdm/ref/collection/p245801coll10/id/584754.

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Bioengineering;
Ph.D.;
Metastasis is the leading cause of death among cancer patients. The metastatic cascade, during which cancer cells from the primary tumor reach a distant organ and form multiple secondary tumors, consists of a series of events starting with cancer cells invasion through the surrounding tissue of the primary tumor. Invading cells may perform proteolytic degradation of the surrounding extracellular matrix (ECM) and directed migration in order to disseminate through the tissue. Both of the mentioned processes are profoundly affected by several parameters originating from the tumor microenvironment (extrinsic) and tumor cells themselves (intrinsic). However, due to the complexity of the invasion process and heterogeneity of the tumor tissue, the exact effect of many of these parameters are yet to be elucidated. ECM proteolysis is widely performed by cancer cells to facilitate the invasion process through the dense and highly cross-linked tumor tissue. It has been shown in vivo that the proteolytic activity of the cancer cells correlates with the cross-linking level of their surrounding ECM. Therefore, the first part of this thesis seeks to understand how ECM cross-linking regulates cancer cells proteolytic activity. This chapter first quantitatively characterizes the correlation between ECM cross-linking and the dynamics of cancer cells proteolytic activity and then identifies ß1-integrin subunit as a master regulator of this process. Once cancer cells degrade their immediate ECM, they directionally migrate through it. Bundles of aligned collagen fibers and gradients of soluble growth factors are two well-known cues of directed migration that are abundantly present in tumor tissues stimulating contact guidance and chemotaxis, respectively. While such cues direct the cells towards a specific direction, they are also known to stimulate cell cycle progression. Moreover, due to the complexity of the tumor tissue, cells may be exposed to both cues simultaneously, and this co-stimulation may happen in the same or different directions. Hence, in the next two chapters of this thesis, the effect of cell cycle progression and contact guidance-chemotaxis dual-cue environments on directional migration of invading cells are assessed. First, we show that cell cycle progression affects contact guidance and not random motility of the cells. Next, we show how exposure of cancer cells to contact guidance-chemotaxis dual-cue environments can improve distinctive aspects of cancer invasion depending on the spatial conformation of the two cues. In this dissertation, we strive to achieve the defined milestones by developing novel mathematical and experimental models of cancer invasion as well as utilizing fluorescent time-lapse microscopy and automated image and signal processing techniques. The results of this study improve our knowledge about the role of the studied extrinsic and intrinsic cues in cancer invasion.
Temple University--Theses
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4

Yaourtis, Andria. „Innate and anti-cancer drug-induced morphological changes in the human breast cancer cell line MDA-MB-231“. Thesis, The University of Sydney, 2021. https://hdl.handle.net/2123/26409.

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Phenotypic changes in tumour cells is a well-established phenomenon and can happen either naturally or in response to a drug. Such changes in phenotype are often accompanied with changes in the behaviour of tumour cells, including growth, proliferation, as well as their migratory and invasive capacity. Phenotypic changes can, therefore, impact the aggressiveness of the tumour cell and dictate their metastatic potential. Thus, it is of utmost importance to fully understand and characterise phenotypic changes in tumour cells in order to better understand tumour progression and identify therapeutic targets. The research described in this thesis focused on morphological changes in the human breast cancer cell line, MDA-MB-231, arising from two conditions: a spontaneous, natural transformation that cells undergo, and a transformation induced by the gallium complex, tris(8-hydroxyquinolinato)gallium(III) [GaQ3]. Techniques utilised in this study included digital holographic microscopy, scanning electron microscopy, confocal microscopy, short tandem repeat profiling, migration and invasion wound healing assays, as well as Fourier transform infrared spectroscopy. It was found that whether the cell undergoes natural or drug-induced morphological changes, the changes in cell phenotypes are accompanied with functional changes, with the most significant functional change being a reduction in the cell’s invasive potential. Further, phenotypic changes that MDA-MB-231 cells may naturally undergo were likely to be induced by the release and uptake of extracellular vesicles. The findings of this thesis, therefore, have significant implications in understanding cancer metastasis, and opens new avenues for the intervention of possible anti-metastatic therapies.
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Lymburner, Sylvia. „Zinc inhibits magnesium-mediated human breast cancer MDA-MB-231 cell migration on fibronectin“. Thesis, University of British Columbia, 2011. http://hdl.handle.net/2429/37064.

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Breast cancer is the most prevalent type of cancer in Canadian women and ranks second in mortality. The cause of breast cancer deaths is the tumor growth in secondary locations. Zinc has been suggested to alter the affinity by which cells attach to the extracellular matrix. The strength of cell adhesion is paramount to the ability of cancerous cells to migrate. The hypothesis for my thesis research was that zinc promotes the metastasic potential of human breast cancer cells. The overall objective of my thesis research was to characterize the effects of zinc on the growth and metastatic potential of human breast cancer cells. Breast carcinoma MDA-MB-231 cells were cultured in DMEM plus 10% Chelex-100 treated FBS supplemented with 0 (zinc-deficient medium), 5 (zinc-adequate medium), or 25 (zinc-supplemented medium) µmol/L of Zn²⁺ as ZnSO₄. After culture for 96 h, the cells were harvested for determining total cellular zinc concentration, abundance of the labile intracellular pool of zinc, and cell growth. The metastatic potential of the cells was assessed by a combination of migration rate assessed using the wound-healing assay and migration distance using the single cell migration assay. The cells were also assessed for their adhesion on fibronectin, for the involvement of specific integrin subunits using blocking antibody, and integrin activation using FACS. Zinc treatments had no effect on total cellular zinc concentration, cell growth, and viability and essentially had no effect on abundance of the labile intracellular pool of zinc. Zinc as low as 5 µmol/L inhibited MDA-MB-231 cell migration on fibronectin, reduced magnesium-mediated promotion of adhesion and thus was likely involved in inhibiting magnesium-mediated integrin activation. With the use of blocking antibodies, it was determined that α5/β1 integrin was responsible for the adhesion of the cells to fibronectin and it was likely that zinc inhibited adhesion by blocking the activation of this specific form of integrin. Together these results suggested that zinc was an inhibitor of MDA-MB-231 migration on fibronectin, and thus likely an inhibitor of metastases, contrary to the hypothesis.
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6

Esmaeili, Pourfarhangi Kamyar. „Movie11: FUCCI-MDA-MB-231 cells migration in 3D collagen with random fiber architecture“. Diss., Temple University Libraries, 2019. http://cdm16002.contentdm.oclc.org/cdm/ref/collection/p245801coll10/id/584757.

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Bioengineering;
Ph.D.;
Metastasis is the leading cause of death among cancer patients. The metastatic cascade, during which cancer cells from the primary tumor reach a distant organ and form multiple secondary tumors, consists of a series of events starting with cancer cells invasion through the surrounding tissue of the primary tumor. Invading cells may perform proteolytic degradation of the surrounding extracellular matrix (ECM) and directed migration in order to disseminate through the tissue. Both of the mentioned processes are profoundly affected by several parameters originating from the tumor microenvironment (extrinsic) and tumor cells themselves (intrinsic). However, due to the complexity of the invasion process and heterogeneity of the tumor tissue, the exact effect of many of these parameters are yet to be elucidated. ECM proteolysis is widely performed by cancer cells to facilitate the invasion process through the dense and highly cross-linked tumor tissue. It has been shown in vivo that the proteolytic activity of the cancer cells correlates with the cross-linking level of their surrounding ECM. Therefore, the first part of this thesis seeks to understand how ECM cross-linking regulates cancer cells proteolytic activity. This chapter first quantitatively characterizes the correlation between ECM cross-linking and the dynamics of cancer cells proteolytic activity and then identifies ß1-integrin subunit as a master regulator of this process. Once cancer cells degrade their immediate ECM, they directionally migrate through it. Bundles of aligned collagen fibers and gradients of soluble growth factors are two well-known cues of directed migration that are abundantly present in tumor tissues stimulating contact guidance and chemotaxis, respectively. While such cues direct the cells towards a specific direction, they are also known to stimulate cell cycle progression. Moreover, due to the complexity of the tumor tissue, cells may be exposed to both cues simultaneously, and this co-stimulation may happen in the same or different directions. Hence, in the next two chapters of this thesis, the effect of cell cycle progression and contact guidance-chemotaxis dual-cue environments on directional migration of invading cells are assessed. First, we show that cell cycle progression affects contact guidance and not random motility of the cells. Next, we show how exposure of cancer cells to contact guidance-chemotaxis dual-cue environments can improve distinctive aspects of cancer invasion depending on the spatial conformation of the two cues. In this dissertation, we strive to achieve the defined milestones by developing novel mathematical and experimental models of cancer invasion as well as utilizing fluorescent time-lapse microscopy and automated image and signal processing techniques. The results of this study improve our knowledge about the role of the studied extrinsic and intrinsic cues in cancer invasion.
Temple University--Theses
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Lima, Benedicto Augusto Vieira. „Avaliação das atividades citotóxicas de alguns complexos fosfínicos de rutênio (Células tumorais MDA-MB 231)“. Universidade Federal de São Carlos, 2010. https://repositorio.ufscar.br/handle/ufscar/6465.

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In this thesis complexes of general formula: [Ru(NS)(bipy)(PP)]PF6 (NS = 2-mercaptopyridine, 2-mercaptopyrimidine, 4,6-dimethyl-2- mercaptopyrimidine and PP = dppf, dppp, dppe); [Ru(pic)(bipy)(PP)]PF6 (pic = picolinate; PP = dppf, dppp, dppe and dppm), [RuCl(bCN)(bipy)(PP)]PF6 (bCN = benzonitrile; PP = dppf and dppe), and [RuCl(bCN)(NN)(dppb)]PF6 (NN = bipy, Mebipy and phen), were synthesised from the precursor complexes cis- [RuCl2(NN)(PP)] and characterized by the usual techniques: 1H and 31P{1H} NMR, IR, UV-Vis, molar conductimetry, elemental analysis, cyclic and differential pulse voltammetry and single-crystal X-ray diffraction (except for the compounds [Ru(pic)(bipy)(dppp)]PF6, [Ru(pic)(bipy)(dppm)]PF6 and [RuCl(bCN)(Mebipy)(dppb)]PF6, which suitable single crystal were not obtained). The 31P{1H} NMR spectras of the new compounds showed that the phosphorus atoms were more deshielded than in the correspondent precursor. The E1/2 values of the complexes containing the ligands NS, pic and bCN were higher than those observed in the precursor complexes. The complexes containing the ligand dppf presented two redox process, which were assigned to the redox pairs FeII/FeIII and RuII/RuIII respectively, according to the results of the kinetics experiments monitored by differential pulse voltammetry and 31P{1H} NMR techniques. The molar conductimetry and elemental analysis assays corroborated the proposed formula and the single-crystal X-ray diffraction study of these complexes confirmed their structures. The νCN in the complexes [RuCl(bCN)(NN)(PP)]PF6 were higher (~+8 cm-1) than that observed in the free ligand (2229 cm-1). Also, it was avaluated in vitro antitumor activity of some of the compounds synthesised herein against mammary cancer cell line (MDA-MB-231), murine sarcoma, as well as against M. tuberculosis (H37Rv); some of them presented high activity.
Neste trabalho foram sintetizados os complexos de fórmula: [Ru(NS)(bipy)(PP)]PF6 (NS = 2-mercaptopiridina, 2-mercaptopirimidina, 4,6- dimetil-2-mercaptopirimidina e PP = dppf, dppp, dppe); [Ru(pic)(bipy)(PP)]PF6 (PP = dppf, dppp, dppe e dppm), [RuCl(bCN)(bipy)(PP)]PF6 (bCN = benzonitrila; PP = dppf e dppe), e [RuCl(bCN)(NN)(dppb)]PF6 (NN = bipy, Mebipy e phen) a partir dos complexos precursores de fórmula cis- [RuCl2(NN)(PP)], e foram caracterizados pelas técnicas de RMN de 1H e 31P{1H}, IV, UV-Vis, condutância molar, análise elementar, voltametrias cíclica e de pulso diferencial e por difração de raios-X de monocristal (à exceção dos compostos [Ru(pic)(bipy)(dppp)]PF6, [Ru(pic)(bipy)(dppm)]PF6, [RuCl(bCN)(Mebipy)(dppb)]PF6, dos quais não se obteve cristais adequados para estudado por difração de raios-X). Os espectros de RMN de 31P{1H} mostraram que ocorre a desblindagem dos átomos de fósforo causada pela coordenação dos ligantes NS, pic e bCN. Os complexos sintetizados apresentaram valores de E1/2 maiores que seus correspondentes precursores, e aqueles contendo a bifosfina dppf apresentaram dois processos redox, que através de experimentos de cinética realizados por voltametria de pulso diferencial e RMN de 31P{1H} puderam ser atribuídos aos pares FeII/FeIII e RuII/RuIII, respectivamente. As medidas de condutância molar e as de análise elementar corroboraram as fórmulas propostas e o estudo dos cristais resolvidos por difração de raios-X confirmaram as estruturas esperadas. Os valores de νCN nos complexos [RuCl(bCN)(NN)(PP)]PF6 foram maiores (~+8 cm-1) que o observado no ligante bCN livre (2229 cm-1). Alguns dos complexos sintetizados neste trabalho também foram avaliados in vitro como agentes antitumorais contra a linhagem de células de câncer de mama MDA-MB-231, sarcoma murino e também como anti-M. tuberculosis (H37Rv); alguns deles mostraram bons resultados.
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8

Esmaeili, Pourfarhangi Kamyar. „Movie12: FUCCI-MDA-MB-231 cells migration in 3D collagen with vertically aligned fiber architecture“. Diss., Temple University Libraries, 2019. http://cdm16002.contentdm.oclc.org/cdm/ref/collection/p245801coll10/id/584747.

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Bioengineering;
Ph.D.;
Metastasis is the leading cause of death among cancer patients. The metastatic cascade, during which cancer cells from the primary tumor reach a distant organ and form multiple secondary tumors, consists of a series of events starting with cancer cells invasion through the surrounding tissue of the primary tumor. Invading cells may perform proteolytic degradation of the surrounding extracellular matrix (ECM) and directed migration in order to disseminate through the tissue. Both of the mentioned processes are profoundly affected by several parameters originating from the tumor microenvironment (extrinsic) and tumor cells themselves (intrinsic). However, due to the complexity of the invasion process and heterogeneity of the tumor tissue, the exact effect of many of these parameters are yet to be elucidated. ECM proteolysis is widely performed by cancer cells to facilitate the invasion process through the dense and highly cross-linked tumor tissue. It has been shown in vivo that the proteolytic activity of the cancer cells correlates with the cross-linking level of their surrounding ECM. Therefore, the first part of this thesis seeks to understand how ECM cross-linking regulates cancer cells proteolytic activity. This chapter first quantitatively characterizes the correlation between ECM cross-linking and the dynamics of cancer cells proteolytic activity and then identifies ß1-integrin subunit as a master regulator of this process. Once cancer cells degrade their immediate ECM, they directionally migrate through it. Bundles of aligned collagen fibers and gradients of soluble growth factors are two well-known cues of directed migration that are abundantly present in tumor tissues stimulating contact guidance and chemotaxis, respectively. While such cues direct the cells towards a specific direction, they are also known to stimulate cell cycle progression. Moreover, due to the complexity of the tumor tissue, cells may be exposed to both cues simultaneously, and this co-stimulation may happen in the same or different directions. Hence, in the next two chapters of this thesis, the effect of cell cycle progression and contact guidance-chemotaxis dual-cue environments on directional migration of invading cells are assessed. First, we show that cell cycle progression affects contact guidance and not random motility of the cells. Next, we show how exposure of cancer cells to contact guidance-chemotaxis dual-cue environments can improve distinctive aspects of cancer invasion depending on the spatial conformation of the two cues. In this dissertation, we strive to achieve the defined milestones by developing novel mathematical and experimental models of cancer invasion as well as utilizing fluorescent time-lapse microscopy and automated image and signal processing techniques. The results of this study improve our knowledge about the role of the studied extrinsic and intrinsic cues in cancer invasion.
Temple University--Theses
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9

Whitehurst, Brandt D. „VEGF-A modulates lymphangiogenic mechanisms in an orthotopic model of human breast carcinoma MDA-MB-231 /“. Available to subscribers only, 2006. http://proquest.umi.com/pqdweb?did=1136079881&sid=25&Fmt=2&clientId=1509&RQT=309&VName=PQD.

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Thesis (M.S.)--Southern Illinois University Carbondale, 2006.
"Department of Molecular Biology, Microbiology and Biochemisty." Includes bibliographical references (leaves 52-71). Also available online.
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Luvizon, Aline Carbonera [UNESP]. „Mecanismo de ação do estrógeno no gene Amphiregulin em células MCF7 e MDA-MB-231 via P13K“. Universidade Estadual Paulista (UNESP), 2014. http://hdl.handle.net/11449/123271.

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Conselho Nacional de Desenvolvimento Científico e Tecnológico (CNPq)
A importância do estrógeno (E2) no desenvolvimento do câncer de mama é bem estabelecido na literatura. O uso de antagonistas de E2 para o tratamento de tumores positivos para o receptor de estrógeno mostra-se importante para a sobrevida de pacientes acometidas pela doença. Amphiregulin (Areg), um fator de crescimento regulador multifuncional que pode ser induzido por estrógeno, possui papel central no desenvolvimento da glândula mamária e na morfogênese de órgãos e é expresso tanto em tecidos normais como cancerosos. Estudos clínicos sugerem que amphiregulin também desempenha papel importante na progressão do câncer da mama humano e a sua expressão aumentada tem sido associada com doença agressiva. Para investigar o mecanismo pelo qual o E2 induz a expressão de AREG, células MCF-7 e MDA-MB-231 foram tratadas durante 10 minutos, 30 minutos, 1 hora e 4 horas com veículo (controle) ou E2 isoladamente ou em associação com Fulvestrant (ICI, inibidor do receptor de estrógeno), Actinomicina D (ACTD, inibidor da transcrição gênica), Ciclohexamida (CHX, inibidor da síntese proteica) ou LY (inibidor da via PI3K). Os inibidores também foram utilizados isoladamente. O RNAm foi extraído das células pelo método de trizol e a expressão de AREG foi analisada por qRT-PCR. O tratamento de ambas as células com E2 induziu aumento do RNAm de AREG em todos os tempos analisados. Esse aumento foi parcialmente dependente de ER nas células MCF-7 nos tempos de 10 minutos, 1 e 4 horas. Em 30 minutos não foi observado a ligação do E2 com o ER para que houvesse o aumento da expressão do gene alvo. Nas células MDA-MB-231 o estrógeno aumentou o RNAm de AREG por pelo menos duas vias distintas em todos tempos analisados. Uma das vias ativa a via PI3K para que este efeito ocorra. Nossos resultados demonstram que o E2 é capaz de induzir a expressão de AREG em linhagens de células de câncer de ...
The relevance of estrogen in breast cancer development is well established in the literature. The use of E2 antagonists for ER-positive breast cancer treatment is shown to be important to patients´ survival. Amphiregulin, a multifunctional growth regulator factor that may be induced by estrogen plays a central role in development of mammary glands and organ morphogenesis, is expressed in both normal and cancerous tissues. Clinical studies suggest that amphiregulin also is important in human breast cancer progression and its expression has been associated with aggressive disease. To investigate the mechanism whereby E2 induces AREG expression, MCF-7 and MDA-MB-231 cells were treated for 10 minutes, 30 minutes, 1 hour or 4 hours with vehicle (control) or estrogen (E2) isolated or in association with Fulvestrant (ICI, estrogen receptor inhibitor), Actinomycin D (ACTD, gene transcription inhibitor), Cycloheximide (CHX, protein synthesis inhibitor ) or LY (PI3K inhibitor). The inhibitors were also used alone. mRNA was extracted from the cells by the Trizol method and AREG expression analyzed by qRT-PCR. Treatment of both cell types with E2 increased AREG mRNA expression at all moments. This increase was partially ER-dependent in MCF- 7 cells at 10 minutes, 1 and 4 hours. At 30 min, no binding of E2 to ER was obseved. In MDA-MB-231 cells, the estrogen-induced AREG mRNA was enhanced by two distinct pathways at the moments analyzed and PI3K pathways participated in one of them. Our results showed that E2 was able to induce the AREG expression in breast cancer cell lines in an ER-dependent and -independent manner
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Bücher zum Thema "MDA-MB-231"

1

Falcioni, Lisa. The role of the phosphatidylinositol-3 kinase-Akt pathway in determining radiation sensivity in the breast cancer cell line MDA-MB 231. Sudbury, Ont: Laurentian University, School of Graduate Studies, 2005.

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Chang, Fu-Jung. Lipid peroxidation in human MDA-MB-231 breast cancer cells enriched in vitro with linoleic acid and conjugated linoleic acid. 1993.

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Buchteile zum Thema "MDA-MB-231"

1

Stark, A. M., R. Mentlein, H. M. Mehdorn und J. Held-Feindt. „Genetisches Profil von Hirn- und Knochen-selektiven MDA-MB-231 Klonen“. In Chirurgisches Forum und DGAV Forum 2010, 17–19. Berlin, Heidelberg: Springer Berlin Heidelberg, 2010. http://dx.doi.org/10.1007/978-3-642-12192-0_7.

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Enokida, Y., Y. Tsuruno, K. Okubo, Y. Yamaoka und E. Takahashi. „Directional Migration of MDA-MB-231 Cells Under O2/pH Gradients“. In Advances in Experimental Medicine and Biology, 169–74. Cham: Springer International Publishing, 2017. http://dx.doi.org/10.1007/978-3-319-55231-6_23.

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Yahara, D., T. Yoshida, Y. Enokida und E. Takahashi. „Directional Migration of MDA-MB-231 Cells Under Oxygen Concentration Gradients“. In Advances in Experimental Medicine and Biology, 129–34. Cham: Springer International Publishing, 2016. http://dx.doi.org/10.1007/978-3-319-38810-6_17.

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Lai, C. I., W. T. Chen, Y. T. Lai und C. M. Lo. „Electrically Assessing the Effect of TGF-β1 on MDA-MB-231 Cells“. In IFMBE Proceedings, 188–91. Cham: Springer International Publishing, 2015. http://dx.doi.org/10.1007/978-3-319-12262-5_52.

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Moissoglu, Konstadinos, Stephen J. Lockett und Stavroula Mili. „Visualizing and Quantifying mRNA Localization at the Invasive Front of 3D Cancer Spheroids“. In Cell Migration in Three Dimensions, 263–80. New York, NY: Springer US, 2023. http://dx.doi.org/10.1007/978-1-0716-2887-4_16.

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AbstractLocalization of mRNAs at the front of migrating cells is a widely used mechanism that functionally supports efficient cell movement. It is observed in single cells on two-dimensional surfaces, as well as in multicellular three-dimensional (3D) structures and in tissue in vivo. 3D multicellular cultures can reveal how the topology of the extracellular matrix and cell-cell contacts influence subcellular mRNA distributions. Here we describe a method for mRNA imaging in an inducible system of collective cancer cell invasion. MDA-MB-231 cancer cell spheroids are embedded in Matrigel, induced to invade, and processed to image mRNAs with single-molecule sensitivity. An analysis algorithm is used to quantify and compare mRNA distributions at the front of invasive leader cells. The approach can be easily adapted and applied to analyze RNA distributions in additional settings where cells polarize along a linear axis.
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Hada, Yuki, Daisuke Yamaguchi, Yoshihisa Yamaoka und Eiji Takahashi. „Further Evidence that Gradients of Extracellular pH Direct Migration of MDA-MB-231 Cells In Vitro“. In Advances in Experimental Medicine and Biology, 373–78. Cham: Springer International Publishing, 2022. http://dx.doi.org/10.1007/978-3-031-14190-4_61.

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Bakhshpour, Monireh, Ayse Kevser Piskin, Handan Yavuz und Adil Denizli. „Preparation of Notch-4 Receptor Containing Quartz Crystal Microbalance Biosensor for MDA MB 231 Cancer Cell Detection“. In Methods in Molecular Biology, 515–33. New York, NY: Springer US, 2021. http://dx.doi.org/10.1007/978-1-0716-1803-5_27.

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Choi, Eun-Ju, Yujiao Tang, Chun Bok Lee, Sun Hee Cheong, Si Heung Sung, Mi-Rae Oh, Se Young Jang, Pyo-Jam Park und Eun-Kyung Kim. „Effect of Taurine on In Vitro Migration of MCF-7 and MDA-MB-231 Human Breast Carcinoma Cells“. In Taurine 9, 191–201. Cham: Springer International Publishing, 2015. http://dx.doi.org/10.1007/978-3-319-15126-7_17.

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Li, Zhong, Jing Li, Baoqing Mo, Chunyan Hu, Huaqing Liu, Hong Qi, Xinru Wang und Jida Xu. „Genistein induces G2/M cell cycle arrest via stable activation of ERK1/2 pathway in MDA-MB-231 breast cancer cells“. In Proceedings of the VIIIth Conference of the International Society for Trace Element Research in Humans (ISTERH), the IXth Conference of the Nordic Trace Element Society (NTES), and the VIth Conference of the Hellenic Trace Element Society (HTES), 2007, 121–29. Dordrecht: Springer Netherlands, 2008. http://dx.doi.org/10.1007/978-1-4020-9056-1_10.

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Boon, Khoo. „The Mesenchymal-Like Phenotype of the MDA-MB-231 Cell Line“. In Breast Cancer - Focusing Tumor Microenvironment, Stem cells and Metastasis. InTech, 2011. http://dx.doi.org/10.5772/20666.

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Konferenzberichte zum Thema "MDA-MB-231"

1

Yu, J., W. Han, J. Kim, J. Lee, E. Ko, E. Kim, H. Moon und D. Noh. „Anoikis-resistant MDA-MB-231 cells: characteristics and pathway analysis.“ In CTRC-AACR San Antonio Breast Cancer Symposium: 2008 Abstracts. American Association for Cancer Research, 2009. http://dx.doi.org/10.1158/0008-5472.sabcs-2062.

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Mollaeian, Keyvan, Yi Liu und Juan Ren. „Investigation of Nanoscale Poroelasticity of Eukaryotic Cells Using Atomic Force Microscopy“. In ASME 2017 Dynamic Systems and Control Conference. American Society of Mechanical Engineers, 2017. http://dx.doi.org/10.1115/dscc2017-5254.

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Intracellular network deformation of the cell plays an important role in cellular shape formation. Recent studies suggest that cell reshaping and deformation due to external forces involves cellular volume, pore size, elasticity, and intracellular filaments polymerization rate changes. This behavior of live cells can be described by poroelastic models because of the porous structure of the cytoplasm. In this study, the poroelasticity of human mammary basel/claudin low carcinoma cell (MDA-MB-231) was investigated using indentation-based atomic force microscopy. The effects of cell deformation (i.e., indentation) rate on the poroelasticity of MDA-MB-231 cells were studied. Specifically, the cell poroelastic behavior (i.e., the diffusion coefficient) was quantified at different indenting velocities (0.2, 2, 10, 20, 100, 200 μm/s) by fitting the force-relaxation curves using a poroelastic model. It was found that the in general the MDA-MB-231 cells behaved poroelastic, and they were less poroelastic (i.e., with lower diffusion coefficient) at higher indenting velocities due to the local stiffening up caused by faster force loads. Poor poroelastic relaxation was observed when the indenting velocity was lower than 10 μm/s due to the intracelluar fluid redistribution during the slow indenting process to equilibrate the intracellular pressure. Moreover, the measurement results showed that the pore size reduction caused by local stiffening at faster indenting velocities is more dominant than the Young’s modulus in affecting the cell poroelasticity.
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Ferreira, Livia C., Juliana R. Lopes, Bruna V. Jardim, Camila Leonel, Gabriela B. Gelaleti, Heloisa C. Caldas, Mario F. Abbud und Debora A. P. C. Zuccari. „Abstract B46: Effective therapeutic response of MDA-MB-231 cell line to rapamycin.“ In Abstracts: AACR-NCI-EORTC International Conference: Molecular Targets and Cancer Therapeutics--Nov 12-16, 2011; San Francisco, CA. American Association for Cancer Research, 2011. http://dx.doi.org/10.1158/1535-7163.targ-11-b46.

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Desai, N., O. D'Cruz und V. Trieu. „Combination Regimens ofnab-Rapamycin (ABI-009) Effective Against MDA-MB-231 Breast-Tumor Xenografts.“ In Abstracts: Thirty-Second Annual CTRC‐AACR San Antonio Breast Cancer Symposium‐‐ Dec 10‐13, 2009; San Antonio, TX. American Association for Cancer Research, 2009. http://dx.doi.org/10.1158/0008-5472.sabcs-09-6106.

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Chan, Jun Yuan, Aminuddin bin Ahmad Kayani, Alan Soo-Beng Khoo und Marini binti Marzuki. „Exposure of MDA-MB-231 Cells to Dielectrophoretic Fields for Electroporation and Cancer Diagnostics“. In 2018 IEEE-EMBS Conference on Biomedical Engineering and Sciences (IECBES). IEEE, 2018. http://dx.doi.org/10.1109/iecbes.2018.8626717.

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de Oliveira Melo, MN, A. Clavelland Ochioni, P. Zancan, A. Passos Oliveira, R. Garrett, S. Baumgartner und C. Holandino. „Viscum album ethanolic extract promotes MDA-MB-231 cell death by glycolytic enzymes inhibition“. In GA – 70th Annual Meeting 2022. Georg Thieme Verlag KG, 2022. http://dx.doi.org/10.1055/s-0042-1759148.

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7

Ryle, James P., Karen M. Molony, Susan McDonnell, Thomas J. Naughton und John T. Sheridan. „Multispectral lensless digital holographic microscope: imaging MCF-7 and MDA-MB-231 cancer cell cultures“. In SPIE Optical Engineering + Applications, herausgegeben von Khan M. Iftekharuddin und Abdul A. S. Awwal. SPIE, 2009. http://dx.doi.org/10.1117/12.826882.

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8

Strelchuk, Christine, und Holly Jones Taggart. „Abstract 2427: Alterations in gene expression after exposure of MDA-MB-231 cells to isobutylparaben“. In Proceedings: AACR Annual Meeting 2017; April 1-5, 2017; Washington, DC. American Association for Cancer Research, 2017. http://dx.doi.org/10.1158/1538-7445.am2017-2427.

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9

Bachmeier, Beatrice E., Peter H. Killian, Emanuel Kronski und Thomas Efferth. „Abstract 709: Development of resistance towards artesunate in MDA-MB-231 human breast cancer cells“. In Proceedings: AACR 102nd Annual Meeting 2011‐‐ Apr 2‐6, 2011; Orlando, FL. American Association for Cancer Research, 2011. http://dx.doi.org/10.1158/1538-7445.am2011-709.

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10

Bauerschmitz, G., JW Hellinger, G. Emons und C. Gründker. „Reduzierte CTGF Expression in invasiven MDA-MB-231 Mammakarzinomzellen durch Behandlung mit GnRH Agonist Triptorelin“. In 62. Kongress der Deutschen Gesellschaft für Gynäkologie und Geburtshilfe – DGGG'18. Georg Thieme Verlag KG, 2018. http://dx.doi.org/10.1055/s-0038-1670998.

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