Journal articles: 'MCF-7 cells'

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Men, Xin, Mengyang Su, Jun Ma, Yueyang Mou, Penggao Dai, Chao Chen, and Xi An Cheng. "Overexpression of TMEM47 Induces Tamoxifen Resistance in Human Breast Cancer Cells." Technology in Cancer Research & Treatment 20 (January 1, 2021): 153303382110049. http://dx.doi.org/10.1177/15330338211004916.

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Background: Tamoxifen (TAM) is the eminent first-line drug for endocrine therapy of hormone receptor positive premenopausal breast cancer and reduces the risk of recurrence by ∼50%. However, many patients developed TAM resistance and their diseases recurred. Our previous study on transcriptome profile of TAM resistant breast cancer cells revealed that the TMEM47 is one of the most significantly differentially expressed genes. The mechanism of how TMEM47 is involved in TAM resistance was not known. Methods: We constructed a mammal breast cancer cell line, in which TMEM47 was stably overexpressed (TMEM47-OE/MCF-7), to further verify the role of TMEM47 in TAM resistance. siRNA targeting TMEM47 was transfected into TAMR / MCF-7 cells by Liposome. TMEM47 expression was validated on mRNA and protein level by qRT-PCR and western blotting. We tested the cytotoxicity of TAM in the cells. Apoptosis was detected by flow cytometry. Results: Compared to the MCF7 cells, TMEM47 mRNA was significantly up regulated more than 6 folds in the TAMR/MCF7 cells and so its protein. TMEM47 expression level in TMEM47-OE/MCF-7 was similar as in the TAMR/MCF-7 cells. The 50% inhibitory concentration (IC50) value (mean ± SD) of TAM in MCF-7, TAMR/MCF-7 and TMEM47-OE/MCF-7 cells was 1.58 ± 0.19, 2.74 ± 0.24 and 3.12 ± 0.32 µγ/mL, respectively. The apoptosis rates of TAMR/MCF-7 and TMEM47-OE/MCF-7 cell lines were significantly lower than that of MCF-7 cells. After 24 and 48 hours TAM treatments, cell viability was significantly inhibitied in TMEM47 knockdown TAMR/MCF7 cells (P < 0.01). Consistant with the decreased cell viability, the apoptosis rate in TMEM47 knockdown TAMR/MCF-7 cells was significantly increased. Conclusions: Our results suggest that overexpression of TMEM47 in MCF-7 cells acquired TAM resistance to those cells, and knockdown of TMEM47 in TAMR/MCF-7 cells reversed their resistance to TAM. TMEM47 might confer TAM resistance on MCF-7 cells through the inhibition of apoptosis.

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Yang, Seungwon, and Hyun-Man Kim. "ROCK Inhibition Activates MCF-7 Cells." PLoS ONE 9, no. 2 (February 11, 2014): e88489. http://dx.doi.org/10.1371/journal.pone.0088489.

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Chehkun, V. F., T. Borikun, and N. Yu Lukianova. "EFFECT OF 5-AZACYTIDINE ON miRNA EXPRESSION IN HUMAN BREAST CANCER CELLS WITH DIFFERENT SENSITIVITY TO CYTOSTATICS." Experimental Oncology 38, no. 1 (March 22, 2016): 26–30. http://dx.doi.org/10.31768/2312-8852.2016.38(1):26-30.

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Aim: To analyze expression of miRNA in human breast cancer cells, sensitive and resistant to cisplatin and doxorubicin, and to explore possible modification of drug sensitivity via treatment of cells with 5-azacytidine (5-aza), a demethylating agent. Materials and Methods: The study was performed on wild-type MCF-7 cell line (MCF-7/S) and its two sublines MCF-7/Dox and MCF-7/DDP resistant to doxorubicin and cisplatin, respectively. Cells were treated with 5-aza, cisplatin, doxorubicin and their combinations. Relative expression levels of miRNA-221, -200b, -320a, -10b, -34a, -122 and -29b were examined, using qRT-PCR. The MTT assay was used to monitor cell viability. Results: We compared miRNA expression profiles in MCF-7/S and drug resistant MCF-7/Dox and MCF-7/DDP cells. Changes of miRNA-221, -200b, -320a, -10b, -34a, -122 and -29b were observed in both resistant cell lines. The most significant differences were found for miRNA-200b (decreased in 50.0 ± 2.6 and 63.0 ± 3.1 times for MCF-7/Dox and MCF7/DDP cells, respectively) and for oncogenic miRNA-221 levels (increase in 62.0 ± 5.7 times for MCF-7/Dox and 83.8 ± 7.2 times for MCF-7/DDP cells). 5-aza treatment caused an increase of miRNA-10b, -122, -200b levels in MCF-7/S cells, miRNA-34a, -10b, -122, -200b and -320a levels in MCF-7/Dox cells and miRNA-34a, -10b, -200b and -320a levels in MCF-7/DDP cells. Pretreatment of all studied lines with 5-aza resulted in the increase of their sensitivity to studied cytostatics. In particular, the IC50 of doxorubicin decreased by 2-, 4- and 3-fold for cell lines MCF-7/S, MCF-7/Dox and MCF-7/DDP cells, respectively, and IC50 of cisplatin in studied cultures decreased by 3-, 2- and 1.5-fold, respectively. Conclusions: It was shown that use of 5-aza can modify sensitivity of breast cancer cells to cytotoxic drugs not only by it’s demetylation effect, but also by changes in expression of miRNAs, involved in cell proliferation, migration and drug resistance development.

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Huang, M., F. Zhang, Y. Xu, H. Wang, S. Lin, and Y. Zhang. "The comparison of epirubicin-treated MCF-7 mammosphere cells to the treated monolayer cells." Journal of Clinical Oncology 27, no. 15_suppl (May 20, 2009): e13542-e13542. http://dx.doi.org/10.1200/jco.2009.27.15_suppl.e13542.

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e13542 Objective: To explore the different effects of epirubicin on the MCF-7 mammosphere cells and the monolayer cells. Methods: MCF-7 cells were cultured in suspension to generate primary mammospheres. The inhibitory effects of epirubicin on MCF-7 mammosphere cells and the monolayer cells by were measured by MTT assay. The change of CD44+CD24- expression and cell cycle distribution in MCF-7 mammosphere cells and the monolayer cells under epirubicin condition was analyzed by flow cytometry. Results: The cell inhibition was lower in MCF-7 mammosphere cells than that in the monolayer cells when induced by the same concentration of epirubicin (>100 ng/ml),(P<0.01). The CD44+CD24- expression was significantly higher in MCF-7 mammosphere cells than that in the monolayer cells under 400 ng/μl epirubicin for 72 h, (22.8% ± 4.8% Vs 3.3% ± 0.8%),(P<0.01). The cell cycle indicated that MCF-7 mammosphere cells had higher proportion of G0/G1 phase than the monolayer cells, (74.33% ± 3.20% Vs 53.40% ± 3.45%) (P<0.01). Epirubicin had little effect on the G0/G1 phase of MCF-7 mammosphere cells and the monolayer cells, but the S phase and G2 phase was not the case. Conclusion: Epirubicin had lower inhibitory effects on MCF-7 mammosphere cells and it can be used to enrich breast cancer stem cell. Epirubicin had lower effect on the G0/G1 phase of MCF-7 mammosphere cells as compared with control. No significant financial relationships to disclose.

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Alkreathy, Huda Mohammed, Noura Farraj AlShehri, Fatemah Omer Kamel, Ahmed Khalaf Alghamdi, Ahmed Esmat, and Shahid Karim. "Aged garlic extract potentiates doxorubicin cytotoxicity in human breast cancer cells." Tropical Journal of Pharmaceutical Research 19, no. 8 (November 19, 2020): 1669–76. http://dx.doi.org/10.4314/tjpr.v19i8.15.

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Purpose: To investigate the potential chemo-sensitizing effect of aged garlic extract (AGE) on doxorubicin (DOX) in breast cancer cells (MCF-7), and the possible underlying mechanisms.Methods: Human breast cancer cell line (MCF-7) was treated with AGE and DOX. The cytotoxic effects of AGE and DOX were investigated via cell cycle analysis and apoptosis induction, using flow cytometry. Mechanistic studies involved the determination of cellular uptake of DOX and p-glycoprotein (P-gp) activity.Results: Combined treatment of MCF7 cells with AGE and DOX produced no significant effect at AGE dose of 10 mg/mL. However, co-treatment with AGE at doses of 50 and 93 mg/mL enhanced the cytotoxicity of DOX on MCF-7 cells, with IC50 values of 0.962 and 0.999 μM, respectively, whencompared with 1.85 μM DOX alone. Moreover, Annexin V-FITC and PI techniques showed that AGE significantly increased percentage of cells in late apoptosis. Besides, AGE-DOX treatment significantly increased cellular uptake of DOX and inhibited P-gp activity, when compared with DOX alone (p < 0.05).Conclusion: AGE enhances the cytotoxic effect of DOX on MCF-7 cells, most likely due to cell cycle distribution, stimulation of apoptosis, increased uptake of DOX by MCF7, and inhibition of P-gp activity. Keywords: Aged garlic extract, Doxorubicin, Breast cancer, MCF-7 cell line, P-glycoprotein, Apoptosis, Cell cycle

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Gelmann, Edward P., Erik W. Thompson, and Connie L. Sommers. "Invasive and metastatic properties of MCF-7 cells andrasH-transfected MCF-7 cell lines." International Journal of Cancer 50, no. 4 (February 20, 1992): 665–69. http://dx.doi.org/10.1002/ijc.2910500431.

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Kars, Meltem Demirel, Özlem Darcansoy Iseri, Ali Ugur Ural, Ferit Avcu, Murat Beyzadeoglu, Bahar Dirican, and Ufuk Gündüz. "Development of radioresistance in drug resistant human MCF-7 breast cancer cells." Journal of Radiotherapy in Practice 8, no. 4 (December 2009): 207–13. http://dx.doi.org/10.1017/s1460396909990070.

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AbstractBackground and purpose: Radiotherapy is used for the treatment of malignant tumours, and may be used as the primary therapy. It is also common to combine radiotherapy with surgery, chemotherapy, hormone therapy or some combination of them. Even if the tumour is treated intensively, women diagnosed with breast cancer may develop a recurrence. Most recurrences may be in the form of distant metastases, development of multi-drug resistance phenotype or both together. This study demonstrated that some of the multi-drug resistant cancer cells may also become radioresistant.Materials and Methods: Chemoresistance in paclitaxel (MCF-7/Pac), docetaxel (MCF-7/Doc), vincristine (MCF-7/Vinc), doxorubicin (MCF-7/Dox) and zoledronic acid (MCF-7/Zol) resistant MCF-7 cells were demonstrated by XTT assay. MDR1 gene expression was detected by real-time PCR in human MCF-7 breast cancer cells. Drug resistant and sensitive cells were exposed to γ-radiation and development of radioresistance was investigated.Results: Results have indicated that paclitaxel, docetaxel, vincristine, doxorubicin and zoledronic acid–selected cells gained varying degrees of resistance to their selective drugs when compared with original MCF-7/S. MCF-7/Pac, MCF-7/Doc, MCF-7/Vinc and MCF-7/Dox cells have all acquired MDR1 expression. Among the resistant sub-lines, MCF-7/Pac and MCF-7/Doc cells were significantly cross-resistant to irradiation compared to the sensitive cells.Conclusion: MCF-7/Pac and MCF-7/Doc cell lines were found radioresistant to γ-radiation. On the contrary, doxorubicin, vincristine and zoledronic acid resistant cancer cells were still sensitive to radiation.

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Song, Ting, Furong Liang, Zhichao Zhang, Yubo Liu, Hongkun Sheng, and Mingzhou Xie. "S1 kills MCF-7/ADR cells more than MCF-7 cells: A protective mechanism of endoplasmic reticulum stress." Biomedicine & Pharmacotherapy 67, no. 8 (October 2013): 731–36. http://dx.doi.org/10.1016/j.biopha.2013.03.015.

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Putri, Dyaningtyas Dewi Pamungkas, Sarmoko Sarmoko, Rifki Febriansah, Endah Puspitasari, Nur Ismiyati, and Aditya Fitriasari. "MCF-7 Resistant Doxorubicin are Characterized by Lamelapodia, Strong Adhesion on Substrate and P-gp Overexpression." Indonesian Journal of Cancer Chemoprevention 2, no. 3 (October 31, 2011): 304. http://dx.doi.org/10.14499/indonesianjcanchemoprev2iss3pp304-309.

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The prognosis of breast cancer patients is closely associated with the response of tumor cells to chemotherapy agent. Doxorubicin is one of the primary chemotherapeutic agents used for the treatment of breast cancer. Resistance to chemotherapy is believed to cause treatment failure in cancer patients. Furthermore, long time exposure to chemotherapeutic agent induces cancer cells resistance. MCF-7 sensitive cells used as chemoresistance model have overexpression P-gp (P-glycoprotein). Chemoresistance was established by treating MCF-7 cells with 0.5 µg/ml doxorubicin-contained medium for a week. 50% inhibiting concentration (IC50) doxorubicin on MCF-7 cells/DOX were determined using MTT assay. Western blot assay and immunocytochemistry assay was performed to determine the expression of P-gp. Morphological of MCF-7 cell/DOX was changing to become larger and have lamellapodia. IC50 value of doxorubicin was 700 nM on MCF-7/DOX and 400 nM on sensitive MCF-7 cells. The MCF-7/DOX sensitivity to doxorubicin was decreased, shown by 1.5 fold higher IC50 of doxorubicin on MCF-7/DOX compared to MCF-7 sensitive cells. Treatment doxorubicin to sensitive MCF-7 cells leads to the increasing P-gp expression. The P-gp level expression has strong correlation with the low sensitivity of MCF-7/DOX to doxorubicin.Keywords: doxorubicin, resistance cells, sensitive MCF-7 cell

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Guo, Qingming, Danni Zhu, Xiaocui Bu, Xiaofang Wei, Changyou Li, Daiqing Gao, Xiaoqiang Wei, Xuezhen Ma, and Peng Zhao. "Efficient killing of radioresistant breast cancer cells by cytokine-induced killer cells." Tumor Biology 39, no. 3 (March 2017): 101042831769596. http://dx.doi.org/10.1177/1010428317695961.

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Recurrence of breast cancer after radiotherapy may be partly explained by the presence of radioresistant cells. Thus, it would be desirable to develop an effective therapy against radioresistant cells. In this study, we demonstrated the intense antitumor activity of cytokine-induced killer cells against MCF-7 and radioresistant MCF-7 cells, as revealed by cytokine-induced killer–mediated cytotoxicity, tumor cell proliferation, and tumor invasion. Radioresistant MCF-7 cells were more susceptible to cytokine-induced killer cell killing. The stronger cytotoxicity of cytokine-induced killer cells against radioresistant MCF-7 cells was dependent on the expression of major histocompatibility complex class I polypeptide–related sequence A/B on radioresistant MCF-7 cells after exposure of cytokine-induced killer cells to sensitized targets. In addition, we demonstrated that cytokine-induced killer cell treatment sensitized breast cancer cells to chemotherapy via the downregulation of TK1, TYMS, and MDR1. These results indicate that cytokine-induced killer cell treatment in combination with radiotherapy and/or chemotherapy may induce synergistic antitumor activities and represent a novel strategy for breast cancer.

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Habibnejad Korayem, Moharam, and Zahra Rastegar. "Experimental Characterization of MCF-10A Normal Cells Using AFM: Comparison with MCF-7 Cancer Cells." Molecular & Cellular Biomechanics 16, no. 2 (2019): 109–22. http://dx.doi.org/10.32604/mcb.2019.04706.

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Zuka, Masahiko, Yunchao Chang, Zhaoyi Wang, James R. Berenson, and Thomas F. Deuel. "Pleiotrophin Secreted from Human Breast Cancer MCF-7-Ptn Cells Activates Stromal Fibroblasts, Induces Epithelial Island Formation, and Remodels the Microenvironment." Blood 108, no. 11 (November 16, 2006): 2568. http://dx.doi.org/10.1182/blood.v108.11.2568.2568.

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Abstract Pleiotrophin (PTN, Ptn) is an 18 kD cytokine that is expressed in many human breast cancers and its gene is inappropriately expressed in cell lines derived from these breast cancers. To study the siginificance of inappropriate expression of Ptn in human breast cancer cells on surrounding stromal cells, we first compared nude mouse xenografts of MCF-7 and MCF-7-Ptn cells. MCF-7-Ptn cells lack the Receptor Protein Tyrosine Phosphatase (RPTP)b/z, the PTN receptor, and thus are not responsive to PTN through autocrine or paracrine stimulation. The MCF-7-Ptn cell xenografts grew rapidly whereas MCF-7 cells xenografts were barely detectable 6 weeks after injection. MCF-7-Ptn cells that were co-injected with equal numbers of NIH3T3 cells grew even more rapidly in the flanks of the nude mice. Surprisingly, the MCF-7-Ptn cell explants developed a morphological phenotype remarkably similar to that of the human invasive ductal carcinoma. We then co-cultured MCF-7 cells that express Ptn (MCF-7-Ptn cells) with NIH 3T3 cells. Secretion of PTN from MCF-7-Ptn cells induced formation of sharply defined clusters of MCF-7-Ptn cells, termed “epithelial islands”, that were surrounded by dense fibrous bands interspersed with NIH 3T3 cells that morphologically closely resemble carcinoma associated fibroblasts (CAFs). A striking increase in tropoelastin and expression of type IV procollagen mRNA was identified in NIH3T3 cells co-cultured with MCF-7-Ptn cells. Furthermore, different markers often resulting from stromal cell-carcinoma cell interactions in breast cancer, including protein kinase C (PKC)-d, and both human and murine matrix metalloproteinase (MMP) 9 were identified either in cells or in the culture media taken from MCF-7-Ptn/NIH3T3 cell co-cultures. The induction of these biochemical and morphological features in the co-cultures of MCF-7-Ptn and NIH3T3 cells was demonstrated to be Ptn expression dependent, PTN-secretion dependent, and NIH3T3 cell dependent. The data suggest that PTN secretion alone from human breast cancer cells with inappropriate expression of Ptn is sufficient to markedly remodel the microenvironment of the breast cancer cell and induce a morphological transition of the MCF-7-Ptn cells and NIH3T3 cells to patterns resembling breast carcinomas through activation of the PTN/RPTPb/z signaling pathway in NIH3T3 cells and reciprocal signaling between the carcinoma stromal cells and the PTN secreting breast cancer cells.

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Tsai, Tsuimin, Ruey-Long Hong, Jui-Chang Tsai, Pei-Jen Lou, I.-Fang Ling, and Chin-Tin Chen. "Effect of 5-aminolevulinic acid-mediated photodynamic therapy on MCF-7 and MCF-7/ADR cells." Lasers in Surgery and Medicine 34, no. 1 (January 2004): 62–72. http://dx.doi.org/10.1002/lsm.10246.

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Mealey, Katrina L., Rola Barhoumi, Robert C. Burghardt, Stephen Safe, and Deborah T. Kochevar. "Doxycycline Induces Expression of P Glycoprotein in MCF-7 Breast Carcinoma Cells." Antimicrobial Agents and Chemotherapy 46, no. 3 (March 2002): 755–61. http://dx.doi.org/10.1128/aac.46.3.755-761.2002.

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ABSTRACT P-glycoprotein (P-gp) overexpression by tumor cells imparts resistance to multiple antineoplastic chemotherapeutic agents (multiple drug resistance). Treatment of tumor cells with chemotherapeutic agents such as anthracyclines, epipodophyllotoxins, and Vinca alkaloids results in induction of P-gp expression. This study was performed to determine if clinically relevant antimicrobial drugs (i.e., drugs that are used to treat bacterial infections in cancer patients) other than antineoplastic agents can induce expression of P-gp in MCF-7 breast carcinoma cells. Expression of P-gp and MDR1 mRNA was determined in samples from MCF-7 cells that were treated in culture with doxorubicin (positive control) and the antimicrobial drugs doxycycline, piperacillin, and cefoperazone. The functional status of P-gp was assessed using laser cytometry to determine intracellular doxorubicin concentrations. The MTT (3-[4,5-dimethylthiazol-2-yl]-2,5-diphenyltetrazolium bromide) assay was used to determine if the cytotoxicity of experimental drugs was related to their ability to induce P-gp expression. MCF-7 cells treated with doxycycline (MCF-7/doxy) were stimulated to overexpress P-gp, whereas cells treated with piperacillin and cefoperazone did not overexpress P-gp. MCF-7/doxy cells were compared to a positive-control subline, MCF-7/Adr, previously selected for doxorubicin resistance, and to MCF-7 cells treated with doxorubicin (MCF-7/doxo). All three sublines overexpressed P-gp and MDR1 mRNA and accumulated less intracellular doxorubicin than did control MCF-7 cells. P-gp expression was induced only by experimental drugs that were cytotoxic (doxorubicin and doxycycline). Doxycycline, a drug that has been used for treatment of bacterial infections in cancer patients, can induce functional P-gp expression in cancer cells, resulting in multidrug resistance.

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Sivakumaran, Nivethika, Sameera R. Samarakoon, Achyut Adhikari, Meran K. Ediriweera, Kamani H. Tennekoon, Neelika Malavige, Ira Thabrew, and Ram Lal (Swagat) Shrestha. "Cytotoxic and Apoptotic Effects of Govaniadine Isolated fromCorydalis govanianaWall. Roots on Human Breast Cancer (MCF-7) Cells." BioMed Research International 2018 (July 24, 2018): 1–11. http://dx.doi.org/10.1155/2018/3171348.

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Current breast cancer therapies have limitations in terms of increased drug resistance resulting in short-term efficacy, thus demanding the discovery of new therapeutic agents. In this study, cytotoxic activity and apoptotic effects of govaniadine isolated fromCorydalis govanianaWall. roots were determined on human breast cancer (MCF-7) cells. The SRB assay result revealed that govaniadine led to dose- and time-dependent cytotoxic effect in MCF-7 cells along with less cytotoxicity against MCF-10A cells. Govaniadine-induced apoptosis was also accompanied by upregulation ofBax,p53, andSurvivinmRNA expression as assessed by real time PCR analysis. Flow cytometric analysis with Annexin V and PI staining indicated that govaniadine is a potent inducer of apoptosis in MCF-7 cell lines. Distinctive morphological changes contributed to apoptosis and DNA laddering were observed in govaniadine-treated MCF-7 cells. Caspase-7 was significantly activated in treated MCF-7 cells. Govaniadine-treated MCF-7 cells also showed enhanced levels of intracellular reactive oxygen species (ROS) and glutathione S-transferase (GST) and decreased levels of glutathione (GSH). The results indicate that govaniadine has potent and selective cytotoxic effects against MCF-7 cells and the potential to induce caspase 7 dependent apoptosis in MCF-7 cells by activation of pathways that lead to oxidative stress.

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Yun, Jun, Ling Wang, and Jia Ying Yuan. "The Impact of Tetrahydropalmatine on ⁹⁹Tc^m-MIBI Uptake of Human Breast Cancer MCF-7 Cell." Applied Mechanics and Materials 138-139 (November 2011): 1078–81. http://dx.doi.org/10.4028/www.scientific.net/amm.138-139.1078.

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Objective: To observe the effects of chemosensitizer on expression of P-glycoprotein (P-gp) in multidrug-resistant (MDR) carcinoma cells and the changes of corresponding 99Tcm-MIBI (referring to methoxy isobutyl isonitrile) uptake kinetics. Methods: Firstly, the immunocytochemistry was used to test the experssion level of P-gp in carcinoma cells; then the γ counter was used to test the uptake rate of radioactive precipitation of 99Tcm-MIBI; and finally to do statistical analysis of the test data. Results: The P-gp expression in MCF-7/S cells was negative, while it was strongly positive in MCF-7/ADM cells, and the P-gp expression in MCF-7/ADM cells reduced significantly after the tetrahydropalmatine (Tet) effect. The uptake rate of MCF-7/S cells reached the maximal value (1.39%) after being cultured with 99Tcm-MIBI for 90 minutes, and then it kept in equilibrium. The 99Tcm-MIBI uptake rate of MCF-7/ADM cells had been maintained at low level, being 0.371% after 90 minutes. The 99Tcm-MIBI uptake rate of MCF-7/S cells was higher than that of MCF-7/ADM cells. After the tetrahydropalmatine and verapamil effects, the 99Tcm-MIBI uptake rate of MCF-7/S cells had no significant change, while the 99Tcm-MIBI uptake rate of MCF-7/ADM cells increased by 1.9 times. Conclusion: Tet can reverse the MDR in MCF-7 cells, and the mechanism can achieve the effect of reversing the drug resistance through adjusting down the expression of P-gp in carcinoma cells.

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Choi, Hoo Kyun, Jin Won Yang, Sang Hee Roh, Chang Yeob Han, and Keon Wook Kang. "Induction of multidrug resistance associated protein 2 in tamoxifen-resistant breast cancer cells." Endocrine-Related Cancer 14, no. 2 (June 2007): 293–303. http://dx.doi.org/10.1677/erc-06-0016.

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Acquired resistance to tamoxifen (TAM) is a serious therapeutic problem in breast cancer patients. The transition from chemotherapy-responsive breast cancer cells to chemotherapy-resistant cancer cells is mainly accompanied by the increased expression of multidrug resistance-associated proteins (MRPs). In this study, it was found that TAM-resistant MCF-7 (TAMR-MCF-7) cells expressed higher levels of MRP2 than control MCF-7 cells. Molecular analyses using MRP2 gene promoters supported the involvement of the pregnane X receptor (PXR) in MRP2 overexpression in TAMR-MCF-7 cells. Although CCAAT/enhancer-binding protein β was overexpressed continuously in TAMR-MCF-7 cells, this might not be responsible for the transcriptional activation of the MRP2 gene. In addition, the basal activities of phosphatidylinositol 3-kinase (PI3-kinase) were higher in the TAMR-MCF-7 cells than in the control cells. The inhibition of PI3-kinase significantly reduced both the PXR activity and MRP2 expression in TAMR-MCF-7 cells. Overall, MRP2 induction plays a role in the additional acquisition of chemotherapy resistance in TAM-resistant breast cancer.

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Wang, Wenping, Irene Liparulo, Nicola Rizzardi, Paola Bolignano, Natalia Calonghi, Christian Bergamini, and Romana Fato. "Coenzyme Q Depletion Reshapes MCF-7 Cells Metabolism." International Journal of Molecular Sciences 22, no. 1 (December 28, 2020): 198. http://dx.doi.org/10.3390/ijms22010198.

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Mitochondrial dysfunction plays a significant role in the metabolic flexibility of cancer cells. This study aimed to investigate the metabolic alterations due to Coenzyme Q depletion in MCF-7 cells. Method: The Coenzyme Q depletion was induced by competitively inhibiting with 4-nitrobenzoate the coq2 enzyme, which catalyzes one of the final reactions in the biosynthetic pathway of CoQ. The bioenergetic and metabolic characteristics of control and coenzyme Q depleted cells were investigated using polarographic and spectroscopic assays. The effect of CoQ depletion on cell growth was analyzed in different metabolic conditions. Results: we showed that cancer cells could cope from energetic and oxidative stress due to mitochondrial dysfunction by reshaping their metabolism. In CoQ depleted cells, the glycolysis was upregulated together with increased glucose consumption, overexpression of GLUT1 and GLUT3, as well as activation of pyruvate kinase (PK). Moreover, the lactate secretion rate was reduced, suggesting that the pyruvate flux was redirected, toward anabolic pathways. Finally, we found a different expression pattern in enzymes involved in glutamine metabolism, and TCA cycle in CoQ depleted cells in comparison to controls. Conclusion: This work elucidated the metabolic alterations in CoQ-depleted cells and provided an insightful understanding of cancer metabolism targeting.

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Mehta, K. "Multidrug-Resistant MCF-7 Cells: An Identity Crisis?" CancerSpectrum Knowledge Environment 94, no. 21 (November 6, 2002): 1652—b—1654. http://dx.doi.org/10.1093/jnci/94.21.1652-b.

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Palka, Jerzy A., and James M. Phang. "Prolidase in human breast cancer MCF-7 cells." Cancer Letters 127, no. 1-2 (May 1998): 63–70. http://dx.doi.org/10.1016/s0304-3835(98)00011-1.

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Staßen, T., M. Port, I. Nuyken, and M. Abend. "Radiation‐induced gene expression in MCF‐7 cells." International Journal of Radiation Biology 79, no. 5 (May 2003): 319–31. http://dx.doi.org/10.1080/0955300032000093146.

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Nielsen, Jesper B., and T. H. Rasmussen. "Antiproliferative effect of butyltin in MCF-7 cells." Environmental Research 96, no. 3 (November 2004): 305–10. http://dx.doi.org/10.1016/j.envres.2004.02.001.

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Ghandadi, Morteza, Javad Behravan, Samira Biabani, Sara Abbaspor, and Fatemeh Mosaffa. "MCF-7 and its Multidrug Resistant Variant MCF-7/ADR Overcome TNF Cytotoxicity through Prevention of Reactive Oxygen Species Accumulation." Pharmaceutical Sciences 25, no. 2 (June 30, 2019): 118–23. http://dx.doi.org/10.15171/ps.2019.18.

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Background: Signal transduction of numerous cytokines and growth factors are mediated by reactive oxygen species (ROS). Tumor necrosis factor-α (TNF-α) have stimulated accumulation of ROS in various in vitro studies. MCF-7 and its Adriamycin resistant variant MCF-7/ADR are resistant against TNF-α cytotoxicity. Role of ROS in the resistance of MCF-7 and MCF-7/ADR cells was investigated. Methods: ROS accumulation and viability in MCF-7 and MCF-7/ADR after TNF-α exposure was evaluated using 2',7'-dichlorofluorescein diacetate (DCFH-DA) as a fluorescent probe and 3-[4, 5-dimethylthiazol-2-yl]-2, 5 diphenyltetrazolium bromide (MTT) cytotoxicity assay respectively. Results: ROS level did not change significantly after TNF-α exposure. Induction of ROS accumulation along with TNF-α treatment sensitized these cells to TNF-α toxicity. Conclusion: It can be concluded that lack of ROS accumulation following TNF-α exposure is involved at least by part in the resistance of MCF-7 and its drug resistant derivative MCF-7/ADR cells to TNF-α cytotoxicity.

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Paramanantham, Anjugam, Min Jeong Kim, Eun Joo Jung, Hye Jung Kim, Seong-Hwan Chang, Jin-Myung Jung, Soon Chan Hong, Sung Chul Shin, Gon Sup Kim, and Won Sup Lee. "Anthocyanins Isolated from Vitis coignetiae Pulliat Enhances Cisplatin Sensitivity in MCF-7 Human Breast Cancer Cells through Inhibition of Akt and NF-κB Activation." Molecules 25, no. 16 (August 9, 2020): 3623. http://dx.doi.org/10.3390/molecules25163623.

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Anthocyanins isolated from Vitis coignetiae Pulliat (Meoru in Korea) (AIMs) have various anti-cancer properties by inhibiting Akt and NF-κB which are involved in drug resistance. Cisplatin (CDDP) is one of the popular anti-cancer agents. Studies reported that MCF-7 human breast cancer cells have high resistance to CDDP compared to other breast cancer cell lines. In this study, we confirmed CDDP resistance of MCF-7 cells and tested whether AIMs can overcome CDDP resistance of MCF-7 cells. Cell viability assay revealed that MCF-7 cells were more resistant to CDDP treatment than MDA-MB-231 breast cancer cells exhibiting aggressive and high cancer stem cell phenotype. AIMs significantly augmented the efficacy of CDDP with synergistic effects on MCF-7 cells. Molecularly, Western blot analysis revealed that CDDP strongly increased Akt and moderately reduced p-NF-κB and p-IκB and that AIMs inhibited CDDP-induced Akt activation, and augmented CDDP-induced reduction of p-NF-κB and p-IκB in MCF-7 cells. In addition, AIMs significantly downregulated an anti-apoptotic protein, XIAP, and augmented PARP-1 cleavage in CDDP-treated MCF-7 cells. Moreover, under TNF-α treatment, AIMs augmented CDDP efficacy with inhibition of NF-κB activation on MCF-7 cells. In conclusion, AIMs enhanced CDDP sensitivity by inhibiting Akt and NF-κB activity of MCF-7 cells that show relative intrinsic CDDP resistance.

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Cory, Ann H., and Joseph G. Cory. "Comparison of the properties of human breast cancer cells: mcf-7 and mcf-7 cells selected for resistance to etoposide." Advances in Enzyme Regulation 41, no. 1 (May 2001): 177–88. http://dx.doi.org/10.1016/s0065-2571(00)00012-1.

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Heydarian, Ashkan, Dornaz Milani, and Seyyed Mohammad Moein Fatemi. "An investigation of the viscoelastic behavior of MCF-10A and MCF-7 cells." Biochemical and Biophysical Research Communications 529, no. 2 (August 2020): 432–36. http://dx.doi.org/10.1016/j.bbrc.2020.06.010.

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Chang, Ching-Yao, Hong-Lin Chan, Hui-Yi Lin, Tzong-Der Way, Ming-Ching Kao, Ming-Zhang Song, Ying-Ju Lin, and Cheng-Wen Lin. "Rhein Induces Apoptosis in Human Breast Cancer Cells." Evidence-Based Complementary and Alternative Medicine 2012 (2012): 1–8. http://dx.doi.org/10.1155/2012/952504.

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Human breast cancers cells overexpressing HER2/neuare more aggressive tumors with poor prognosis, and resistance to chemotherapy. This study investigates antiproliferation effects of anthraquinone derivatives of rhubarb root on human breast cancer cells. Of 7 anthraquinone derivatives, only rhein showed antiproliferative and apoptotic effects on both HER2-overexpressing MCF-7 (MCF-7/HER2) and control vector MCF-7 (MCF-7/VEC) cells. Rhein induced dose- and time-dependent manners increase in caspase-9-mediated apoptosis correlating with activation of ROS-mediated activation of NF-κB- and p53-signaling pathways in both cell types. Therefore, this study highlighted rhein as processing anti-proliferative activity against HER2 overexpression or HER2-basal expression in breast cancer cells and playing important roles in apoptotic induction of human breast cancer cells.

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Kiss, Z., M. Tomono, and W. B. Anderson. "Phorbol ester selectively stimulates the phospholipase D-mediated hydrolysis of phosphatidylethanolamine in multidrug-resistant MCF-7 human breast carcinoma cells." Biochemical Journal 302, no. 3 (September 15, 1994): 649–54. http://dx.doi.org/10.1042/bj3020649.

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The phospholipase D (PLD)-mediated synthesis of phosphatidylethanol (PtdEtOH) and the hydrolysis of phosphatidylethanolamine (PtdEtn) and phosphatidylcholine (PtdCho) were examined in drug-sensitive and multidrug-resistant lines of MCF-7 human breast carcinoma cells. In drug-sensitive (MCF-7/WT) cells, the protein kinase C (PKC) activator phorbol 12-myristate 13-acetate (PMA) failed to enhance either the synthesis of PtdEtOH or the hydrolysis of either phospholipid. In the drug-resistant (MCF-7/MDR) cells, 100 nM PMA greatly enhanced both the synthesis of PtdEtOH (approximately 21-fold) and the hydrolysis of PtdEtn (approximately 29-fold), but had no effect on the hydrolysis of PtdCho. The PLD activators sphingosine and H2O2 were found to elicit only a slight (1.28-1.4-fold) stimulatory effect on PtdCho hydrolysis in both the MCF-7/WT and MCF-7/MDR cell types, and had only a small effect on PtdEtn hydrolysis in the MCF-7/WT cells as well. However, these agents significantly (approximately 2.6-3.5-fold) stimulated PtdEtn hydrolysis in the MCF-7/MDR cells. These data indicate that MCF-7/MDR cells contain a PtdEtn-specific PLD activity which can be selectively stimulated by PMA, sphingosine and H2O2.

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Sookvanichsilp, N., and K. Poemsantitham. "Effects of catechin, diclofenac and celecoxib on the proliferation of MCF-7 and LTED MCF-7 cells." Biomedicine & Preventive Nutrition 1, no. 3 (July 2011): 202–6. http://dx.doi.org/10.1016/j.bionut.2011.06.003.

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Thomas, Rachel J., Theresa A. Guise, Juan Juan Yin, Jan Elliott, Nicole J. Horwood, T. John Martin, and Matthew T. Gillespie. "Breast Cancer Cells Interact with Osteoblasts to Support Osteoclast Formation1." Endocrinology 140, no. 10 (October 1, 1999): 4451–58. http://dx.doi.org/10.1210/endo.140.10.7037.

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Abstract Breast cancers commonly cause osteolytic metastases in bone, a process that is dependent upon osteoclast-mediated bone resorption. Recently the osteoclast differentiation factor (ODF), better termed RANKL (receptor activator of NF-κB ligand), expressed by osteoblasts has been cloned as well as its cognate signaling receptor, receptor activator of NFκB (RANK), and a secreted decoy receptor osteoprotegerin (OPG) that limits RANKL’s biological action. We determined that the breast cancer cell lines MDA-MB-231, MCF-7, and T47D as well as primary breast cancers do not express RANKL but express OPG and RANK. MCF-7, MDA-MB-231, and T47D cells did not act as surrogate osteoblasts to support osteoclast formation in coculture experiments, a result consistent with the fact that they do not express RANKL. When MCF-7 cells overexpressing PTH-related protein (PTHrP) were added to cocultures of murine osteoblasts and hematopoietic cells, osteoclast formation resulted without the addition of any osteotropic agents; cocultures with MCF-7 or MCF-7 cells transfected with pcDNAIneo required exogenous agents for osteoclast formation. When MCF-7 cells overexpressing PTHrP were cultured with murine osteoblasts, osteoblastic RANKL messenger RNA (mRNA) levels were enhanced and osteoblastic OPG mRNA levels diminished; MCF-7 parental cells had no effect on RANKL or OPG mRNA levels when cultured with osteoblastic cells. Using a murine model of breast cancer metastasis to bone, we established that MCF-7 cells that overexpress PTHrP caused significantly more bone metastases, which were associated with increased osteoclast formation, elevated plasma PTHrP concentrations and hypercalcaemia compared with parental or empty vector controls.

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Cerny, Jan, Yingwang Liu, Nathan Moore, Glennice Bowen, Anna M. Cerny, Evelyn Kurt-Jones, Susan Erdman, and JeanMarie Houghton. "Mesenchymal Stem Cells (MSC) Promote Aggressive Behavior of Human Breast Cancer Cells (MCF-7) in Vitro- the Role Cytokines (TNF-alpha) and Chemokines." Blood 112, no. 11 (November 16, 2008): 4750. http://dx.doi.org/10.1182/blood.v112.11.4750.4750.

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Abstract The tumor microenvironment contributes to local tumor growth and may set up a metastatic niche for breast cancer cells. We tested the effects of spontaneously transformed murine mesenchymal stem cells (stMSC; Li et al. Cancer Res 2008) on the migration, proliferation and cell cycle of the MCF-7 human breast cancer cell line. MCF-7 cells were collected from plates held at confluence to establish cell cycle arrest and then grown either in control media (50/50 mix of fresh and conditioned MCF-7 media) or modification of stMSC conditioned media (50/50 mix of fresh and stMSC conditioned media with TNF-alpha, anti-TNF-alpha or isotype control). MCF-7 cells were plated at equal concentrations into 24-well dishes to establish near confluent plates. The MCF-7 monolayer was wounded using a pipette tip, and the area evaluated/photographed at 0, 24 and 48 hours (in triplicate). Media was changed daily. Synchronized cultures were grown in control or MSC media for 0, 24 or 48 hours in triplicates and analyzed by FACS for cell cycle status and standard cell counts. MCF-7 cells grown in MSC cultured media healed 49% (based on wound size) while control wound size was 26% healed at 24 hrs (p=0.00591). At 48 hrs, MCF-7 cells exposed to stMSC media showed 95% healing while MCF-7 cells in control media still retained 50% of the original wound size (50% healing; p=0.00002). The exposure MCF-7 grown in control media and MSC media did not differ in cell cycle progression. MSC media increased proliferation of MCF-7 cells at 24, 48 and 72 hours compared to control media. (p<0.002). In a separate experiments media from stMSC exposed to TNF-alpha led to increased healing of MCF-7 monolayer compared to stMSC conditioned media at 24 hrs (59.5% vs 44.5%; p=0.027). Healing was lower in media from stMSC cultured with anti-TNF blocking antibody compared to stMSC conditioned media at 24 hrs (66.6% vs 95.7%; p=0.002). We have also detected that stMSC conditioned media contains very high levels of TNF-alpha, MCP-1, CCL-5 and also high levels of NF-kB activity in stMSC conditioned media. StMSCs produce factors (such as TNF-alpha) that provide breast cancer cells (MCF-7) with migration and growth advantage. Animal experiments assessing the ability stMSCs to contribute to invasion and migration of breast cancer cells are currently underway.

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Cen, Juan, Li Zhang, Fangfang Liu, Feng Zhang, and Bian-Sheng Ji. "Long-Term Alteration of Reactive Oxygen Species Led to Multidrug Resistance in MCF-7 Cells." Oxidative Medicine and Cellular Longevity 2016 (2016): 1–15. http://dx.doi.org/10.1155/2016/7053451.

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Reactive oxygen species (ROS) play an important role in multidrug resistance (MDR). This study aimed to investigate the effects of long-term ROS alteration on MDR in MCF-7 cells and to explore its underlying mechanism. Our study showed both long-term treatments of H2O2 and glutathione (GSH) led to MDR with suppressed iROS levels in MCF-7 cells. Moreover, the MDR cells induced by 0.1 μM H2O2 treatment for 20 weeks (MCF-7/ROS cells) had a higher viability and proliferative ability than the control MCF-7 cells. MCF-7/ROS cells also showed higher activity or content of intracellular antioxidants like glutathione peroxidase (GPx), GSH, superoxide dismutase (SOD), and catalase (CAT). Importantly, MCF-7/ROS cells were characterized by overexpression of MDR-related protein 1 (MRP1) and P-glycoprotein (P-gp), as well as their regulators NF-E2-related factor 2 (Nrf2), hypoxia-inducible factor 1 (HIF-1α), and the activation of PI3K/Akt pathway in upstream. Moreover, several typical MDR mediators, including glutathione S-transferase-π (GST-π) and c-Myc and Protein Kinase Cα (PKCα), were also found to be upregulated in MCF-7/ROS cells. Collectively, our results suggest that ROS may be critical in the generation of MDR, which may provide new insights into understanding of mechanisms of MDR.

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Klinge, Carolyn M., Belinda J. Petri, and Kellianne M. Piell. "Epitranscriptomic Reader HNRNPA2B1 Confers Endocrine Resistance to Breast Cancer Cells." Journal of the Endocrine Society 5, Supplement_1 (May 1, 2021): A807—A808. http://dx.doi.org/10.1210/jendso/bvab048.1643.

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Abstract Despite new combination therapies improving survival of breast cancer patients with estrogen receptor α (ER+) tumors, the molecular mechanisms for endocrine-resistant metastatic disease remain unresolved. HNRNPA2B1 (Heterogeneous Nuclear Ribonucleoprotein A2/B1), an RNA binding protein that functions as reader of the N(6)-methyladenosine (m6A) mark in transcribed RNA, is upregualted in tamoxifen- and fulvestrant-resistant, estrogen receptor (ERα)+ LCC9 and LY2 cells derived from MCF-7 endocrine-sensitive luminal A breast cancer cells (1). The miRNA-seq transcriptome of MCF-7 cells transiently overexpressing HNRNPA2B1 (A2B1) identified gene ontology (GO) pathways including “cellular response to steroid hormone signaling and estradiol” and “positive regulation of protein ser/thr kinase activity”. Modest (~ 4.5-fold) stable HNRNPA2B1 overexpression in MCF-7 cells (MCF-7-A2B1) results in ablation of growth inhibition by 4-hydroxytamoxifen (4-OHT) and fulvestrant. This was not due to loss or decrease of ERα; in fact, ERα was increased. Conversely, transient knockdown of HNRNPA2B1 in LCC9 and LY2 cells sensitized the cells to growth inhibition by 4-OHT and fulvestrant while reducing ERα. MCF-7-A2B1 cells showed increased migration, invasion, clonogenicity, soft agar colony size, and markers of epithelial-to-mesenchymal transition. Like LCC9 cells, MCF-7-A2B1 cells showed activation of AKT and MAPK and high androgen receptor (AR). Treatment of MCF-7-A2B1 cells with either PI3K inhibitor Wortmannin or MEK inhibitor PD98059 inhibited soft agar colony formation and reduced colony size. Knockdown of HNRNPA2B1 in MCF-7-A2B1 reduces clonogenicity, but had no effect on the clonogenicity of either LCC9 or LY2 cells. These data suggest a role for HNRNPA2B1 in promoting the initiation of acquired endocrine-resistance by activating ser/thr kinase growth factor signaling pathways. Selective inhibition of HNRNPA2B1 may be a target to prevent acquistion of endocrine therapy resistance, but not treat established metastatic disease. Reference: (1) Klinge CM, Piell KM, Tooley CS, Rouchka EC. HNRNPA2/B1 is upregulated in endocrine-resistant LCC9 breast cancer cells and alters the miRNA transcriptome when overexpressed in MCF-7 cells. Scientific reports 2019; 9:9430

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Niazvand, Firoozeh, Mahmoud Orazizadeh, Layasadat Khorsandi, Mohammadreza Abbaspour, Esrafil Mansouri, and Ali Khodadadi. "Effects of Quercetin-Loaded Nanoparticles on MCF-7 Human Breast Cancer Cells." Medicina 55, no. 4 (April 22, 2019): 114. http://dx.doi.org/10.3390/medicina55040114.

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Background and objectives: Previous studies have shown anti-tumor activity of quercetin (QT). However, the low bioavailability of QT has restricted its use. This study aimed to assess the toxic effect of QT encapsulated in solid lipid nanoparticles (QT-SLNs) on the growth of MCF-7 human breast cancer cells. Materials and Methods: MCF-7 and MCF-10A (non-tumorigenic cell line) cell lines treated with 25 µmol/mL of QT or QT-SLNs for 48 h. Cell viability, colony formation, oxidative stress, and apoptosis were evaluated to determine the toxic effects of the QT-SLNs. Results: The QT-SLNs with appropriate characteristics (particle size of 85.5 nm, a zeta potential of −22.5 and encapsulation efficiency of 97.6%) were prepared. The QT-SLNs showed sustained QT release until 48 h. Cytotoxicity assessments indicated that QT-SLNs inhibited MCF-7 cells growth with a low IC50 (50% inhibitory concentration) value, compared to the free QT. QT-SLNs induced a significant decrease in the viability and proliferation of MCF-7 cells, compared to the free QT. QT-SLN significantly increased reactive oxygen species (ROS) level and MDA contents and significantly decreased antioxidant enzyme activity in the MCF-7 cells. Following QT-SLNs treatment, the expression of the Bcl-2 protein significantly decreased, whereas Bx expression showed a significant increase in comparison with free QT-treated cells. Furthermore, The QT-SLNs significantly increased apoptotic and necrotic indexes in MCF-7 cells. Viability, proliferation, oxidative stress and apoptosis of MCF-10A cells were not affected by QT or QT-SLNs. Conclusions: According to the results of this study, SLN significantly enhanced the toxic effect of QT against human breast cancer cells.

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Kogai, Takahiko, Emi Ohashi, Megan S. Jacobs, Saima Sajid-Crockett, Myrna L. Fisher, Yoko Kanamoto, and Gregory A. Brent. "Retinoic Acid Stimulation of the Sodium/Iodide Symporter in MCF-7 Breast Cancer Cells Is Meditated by the Insulin Growth Factor-I/Phosphatidylinositol 3-Kinase and p38 Mitogen-Activated Protein Kinase Signaling Pathways." Journal of Clinical Endocrinology & Metabolism 93, no. 5 (May 1, 2008): 1884–92. http://dx.doi.org/10.1210/jc.2007-1627.

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Abstract Context: All-trans retinoic acid (tRA) induces differentiation in MCF-7 breast cancer cells, stimulates sodium/iodide symporter (NIS) gene expression, and inhibits cell proliferation. Radioiodine administration after systemic tRA treatment has been proposed as an approach to image and treat some differentiated breast cancer. Objective: The objective of this work was to study the relative role of genomic and nongenomic pathways in tRA stimulation of NIS expression in MCF-7 cells. Design: We inspected the human NIS gene locus for retinoic acid-responsive elements and tested them for function. The effects of signal transduction pathway inhibitors were also tested in tRA-treated MCF-7 cells and TSH-stimulated FRTL-5 rat thyroid cells, followed by iodide uptake assay, quantitative RT-PCR of NIS, and cell cycle phase analysis. Results: Multiple retinoic acid response elements around the NIS locus were identified by sequence inspection, but none of them was a functional tRA-induced element in MCF-7 cells. Inhibitors of the IGF-I receptor, Janus kinase, and phosphatidylinositol 3-kinase (PI3K), significantly reduced NIS mRNA expression and iodide uptake in tRA-stimulated MCF-7 cells but not FRTL-5 cells. An inhibitor of p38 MAPK significantly reduced iodide uptake in both tRA-stimulated MCF-7 cells and TSH-stimulated FRTL-5 cells. IGF-I and PI3K inhibitors did not significantly reduce the basal NIS mRNA expression in MCF-7 cells. Despite the chronic inhibitory effects on cell proliferation, tRA did not reduce the S-phase distribution of MCF-7 cells during the period of NIS induction. Conclusion: The IGF-I receptor/PI3K pathway mediates tRA-stimulated NIS expression in MCF-7 but not FRTL-5 thyroid cells.

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Ebrahimi Nigjeh, Siyamak, Fatimah Md Yusoff, Noorjahan Banu Mohamed Alitheen, Mehdi Rasoli, Yeap Swee Keong, and Abdul Rahman bin Omar. "Cytotoxic Effect of Ethanol Extract of Microalga,Chaetoceros calcitrans, and Its Mechanisms in Inducing Apoptosis in Human Breast Cancer Cell Line." BioMed Research International 2013 (2013): 1–8. http://dx.doi.org/10.1155/2013/783690.

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Marine microalgae have been prominently featured in cancer research. Here, we examined cytotoxic effect and apoptosis mechanism of crude ethanol extracts of an indigenous microalga,Chaetoceros calcitrans(UPMAAHU10) on human breast cell lines. MCF-7 was more sensitive than MCF-10A with IC50 value of3.00±0.65, whilst the IC50 value of Tamoxifen against MCF-7 was12.00±0.52 μg/mL after 24 hour incubation. Based on Annexin V/Propidium iodide and cell cycle flow cytometry analysis, it was found that inhibition of cell growth by EEC on MCF-7 cells was through the induction of apoptosis without cell cycle arrest. The apoptotic cells at subG0/G1 phase in treated MCF-7 cells at 48 and 72 hours showed 34 and 16 folds increased compared to extract treated MCF-10A cells which showed only 6 and 7 folds increased at the same time points, respectively. Based on GeXP study, EEC induced apoptosis on MCF-7 cells via modulation of CDK2, MDM2, p21Cip1, Cyclin A2, Bax and Bcl-2. The EEC treated MCF-7 cells also showed an increase in Bax/Bcl-2 ratio that in turn activated the caspase-dependent pathways by activating caspase 7. Thus, marine microalga,Chaetoceros calcitransmay be considered a good candidate to be developed as a new anti-breast cancer drug.

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Augimeri, Giuseppina, Giusi La Camera, Luca Gelsomino, Cinzia Giordano, Salvatore Panza, Diego Sisci, Catia Morelli, et al. "Evidence for Enhanced Exosome Production in Aromatase Inhibitor-Resistant Breast Cancer Cells." International Journal of Molecular Sciences 21, no. 16 (August 14, 2020): 5841. http://dx.doi.org/10.3390/ijms21165841.

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Aromatase inhibitors (AIs) represent the standard anti-hormonal therapy for post-menopausal estrogen receptor-positive breast cancer, but their efficacy is limited by the emergence of AI resistance (AIR). Exosomes act as vehicles to engender cancer progression and drug resistance. The goal of this work was to study exosome contribution in AIR mechanisms, using estrogen-dependent MCF-7 breast cancer cells as models and MCF-7 LTED (Long-Term Estrogen Deprived) subline, modeling AIR. We found that exosome secretion was significantly increased in MCF-7 LTED cells compared to MCF-7 cells. MCF-7 LTED cells also exhibited a higher amount of exosomal RNA and proteins than MCF-7 cells. Proteomic analysis revealed significant alterations in the cellular proteome. Indeed, we showed an enrichment of proteins frequently identified in exosomes in MCF-7 LTED cells. The most up-regulated proteins in MCF-7 LTED cells were represented by Rab GTPases, important vesicle transport-regulators in cancer, that are significantly mapped in “small GTPase-mediated signal transduction”, “protein transport” and “vesicle-mediated transport” Gene Ontology categories. Expression of selected Rab GTPases was validated by immunoblotting. Collectively, we evidence, for the first time, that AIR breast cancer cells display an increased capability to release exosomes, which may be associated with an enhanced Rab GTPase expression. These data provide the rationale for further studies directed at clarifying exosome’s role on endocrine therapy, with the aim to offer relevant markers and druggable therapeutic targets for the management of hormone-resistant breast cancers.

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Kochumon, Shihab, Amnah Al-Sayyar, Texy Jacob, Amal Hasan, Fahd Al-Mulla, Sardar Sindhu, and Rasheed Ahmad. "TNF-α Increases IP-10 Expression in MCF-7 Breast Cancer Cells via Activation of the JNK/c-Jun Pathways." Biomolecules 11, no. 9 (September 13, 2021): 1355. http://dx.doi.org/10.3390/biom11091355.

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IP-10 (also called CXCL10) plays a significant role in leukocyte homing to inflamed tissues, and increased IP-10 levels are associated with the pathologies of various inflammatory disorders, including type 2 diabetes, atherosclerosis, and cancer. TNF-α is a potent activator of immune cells and induces inflammatory cytokine expression in these cells. However, it is unclear whether TNF-α is able to induce IP-10 expression in MCF-7 breast cancer cells. We therefore determined IP-10 expression in TNF-α-treated MCF-7 cells and investigated the mechanism involved. Our data show that TNF-α induced/upregulated the IP-10 expression at both mRNA and protein levels in MCF-7 cells. Inhibition of JNK (SP600125) significantly suppressed the TNF-α-induced IP-10 in MCF-7 cells, while the inhibition of p38 MAPK (SB203580), MEK1/2 (U0126), and ERK1/2 (PD98059) had no significant effect. Furthermore, TNF-α-induced IP-10 expression was abolished in MCF-7 cells deficient in JNK. Similar results were obtained using MCF-7 cells deficient in c-Jun. Moreover, the JNK kinase inhibitor markedly reduced the TNF-α-induced JNK and c-Jun phosphorylation. The kinase activity of JNK induced by TNF-α stimulation of MCF-7 cells was significantly inhibited by SP600125. Altogether, our novel findings provide the evidence that TNF-α induces IP-10 expression in MCF-7 breast cancer cells via activation of the JNK/c-Jun signaling pathway.

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Sarighieh, Mehrnaz Asadi, Vahideh Montazeri, Amir Shadboorestan, Mohammad Hossein Ghahremani, and Seyed Nasser Ostad. "The Inhibitory Effect of Curcumin on Hypoxia Inducer Factors (Hifs) as a Regulatory Factor in the Growth of Tumor Cells in Breast Cancer Stem-Like Cells." Drug Research 70, no. 11 (September 22, 2020): 512–18. http://dx.doi.org/10.1055/a-1201-2602.

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AbstractHypoxia in the microenvironment is related to chemotherapy resistance, tumor progression, and metastasis. Curcumin, as a phenolic compound extracted from the turmeric, has been used as an anti-cancer agent with low toxicity in recent years. Since curcumin has inhibitory activities against hypoxia-inducible factors (HIFs) in several cancers, this study was conducted to examine the effect of curcumin on MCF-7 cells and cancer stem-like cells (CS-LCs) under hypoxic and normoxic conditions. CS-LCs were isolated from MCF-7 cells using the magnet activated cell sorting (MACS) method based on CD44 +/ CD24 - surface markers. The effects of curcumin on the viability of MCF-7 cells and CS-LCs were examined in hypoxic and normoxic conditions using the MTT test. The effects of curcumin on apoptosis and cell cycle of CS-LCs and MCF-7 cells were analyzed using flow cytometry. Moreover, the inhibitory effects of curcumin on the levels of HIF-1 and HIF-2α protein in CS-LCs were investigated using the western blot method. Early apoptosis occurred in CSC-LCs more than MCF-7 cells under hypoxic conditions. Flow cytometry assay showed that curcumin caused cell cycle arrest of CSC-LCs and MCF-7 at the G2/M phase under hypoxic conditions while under normoxic conditions, arrest occurred at the G0/G1 phase in MCF-7 cells and at S and G2/M phases in CS-LCs. Based on the results, the curcumin inhibited the expression of HIF-1 by degrading ARNT in CS-LCs.In conclusion, curcumin has inhibitory effects on MCF- 7 cells and CS- LCs and thus may be used as an antitumor agent.

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Choi, Youn Kyung, Sung-Gook Cho, Hyeong Sim Choi, Sang-Mi Woo, Yee Jin Yun, Yong Cheol Shin, and Seong-Gyu Ko. "JNK1/2 Activation by an Extract from the Roots ofMorus albaL. Reduces the Viability of Multidrug-Resistant MCF-7/Dox Cells by Inhibiting YB-1-Dependent MDR1 Expression." Evidence-Based Complementary and Alternative Medicine 2013 (2013): 1–10. http://dx.doi.org/10.1155/2013/741985.

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Cancer cells acquire anticancer drug resistance during chemotherapy, which aggravates cancer disease. MDR1 encoded from multidrug resistance gene 1 mainly causes multidrug resistance phenotypes of different cancer cells. In this study, we demonstrate that JNK1/2 activation by an extract from the root ofMorus albaL. (White mulberry) reduces doxorubicin-resistant MCF-7/Dox cell viability by inhibiting YB-1 regulation ofMDR1gene expression. When MCF-7 or MCF-7/Dox cells, where MDR1 is highly expressed were treated with an extract from roots or leaves ofMorus albaL., respectively, the root extract from the mulberry (REM) but not the leaf extract (LEM) reduced cell viabilities of both MCF-7 and MCF-7/Dox cells, which was enhanced by cotreatment with doxorubicin. REM but not LEM further inhibited YB-1 nuclear translocation and its regulation ofMDR1gene expression. Moreover, REM promoted phosphorylation of c-Jun NH2-terminal kinase 1/2 (JNK1/2) and JNK1/2 inhibitor, SP600125 and rescued REM inhibition of both MDR1 expression and viabilities in MCF-7/Dox cells. Consistently, overexpression of JNK1, c-Jun, or c-Fos inhibited YB-1-dependent MDR1 expression and reduced viabilities in MCF-7/Dox cells. In conclusion, our data indicate that REM-activated JNK-cJun/c-Fos pathway decreases the viability of MCF-7/Dox cells by inhibiting YB-1-dependentMDR1gene expression. Thus, we suggest that REM may be useful for treating multidrug-resistant cancer cells.

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El-Benhawy, Sanaa A., Heba G. El-Sheredy, Heba B. Ghanem, and Amira A. Abo El-Soud. "Berberine can amplify cytotoxic effect of radiotherapy by targeting cancer stem cells." Breast Cancer Management 9, no. 2 (June 1, 2020): BMT41. http://dx.doi.org/10.2217/bmt-2020-0007.

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Aim: Our objective was to investigate the effect of ionizing radiation (IR) and berberine on the expression of stem cell markers OCT4 and SOX2. Materials & methods: The study involved the following groups: Group I: MCF-7 spheroids as untreated control; Group II: MCF-7 spheroids treated with IR; Group III: MCF-7 spheroids treated with berberine; and Group IV: MCF-7 spheroids treated with berberine + IR. MCF-7 spheroids’ metabolic activity and viability was determined with 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyl tetrazolium bromide assay. OCT4 and SOX2 genes expression were assayed by real time-plymerase chain reaction (RT-PCR). Results: IR and berberine treatment decreased the viability of MCF-7 spheroids and reduced OCT4 and SOX2 genes expression. Combining berberine with IR leads to a significant reduction in cell viability and OCT4 and SOX2 genes expression when compared with radiation alone treated group. Conclusion: Berberine showed to be a good candidate for further studies as a new anticancer drug in the treatment of breast cancer. Berberine has a radiosensitizing effect through targeting cancer stem cells.

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Misiura, Magdalena, Ilona Ościłowska, Katarzyna Bielawska, Jerzy Pałka, and Wojciech Miltyk. "PRODH/POX-Dependent Celecoxib-Induced Apoptosis in MCF-7 Breast Cancer." Pharmaceuticals 14, no. 9 (August 29, 2021): 874. http://dx.doi.org/10.3390/ph14090874.

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Celecoxib (Cx), an inhibitor of cyclooxygenase 2, induces apoptosis of cancer cells. However, the mechanism of the chemopreventive effect remains not fully understood. We aimed to investigate the role of PRODH/POX that is involved in the regulation of apoptosis induced by celecoxib. MCF-7 breast cancer cell line and the corresponding MCF-7 cell line with silenced PRODH/POX (MCF-7shPRODH/POX) were used. The effects of Cx on cell viability, proliferation, and cell cycle were evaluated. The expressions of protein markers for apoptosis (Bax, caspase 9, and PARP) and autophagy (Atg5, Beclin 1, and LC3A/B) were investigated by Western immunoblotting. To analyze the proline metabolism, collagen biosynthesis, prolidase activity, proline concentration, and the expression of proline-related proteins were evaluated. The generation of ATP, ROS, and the ratio of NAD+/NADH and NADP+/NADPH were determined to test the effect of Cx on energetic metabolism in breast cancer cells. It has been found that Cx attenuated MCF-7 cell proliferation via arresting the cell cycle. Cx induced apoptosis in MCF-7 breast cancer cells, while in MCF-7shPRODH/POX, autophagy occurred more predominantly. In MCF-7 breast cancer cells, Cx affected proline metabolism through upregulation of proline biosynthesis, PRODH/POX and PYCRs expressions, PEPD activity, and downregulation of collagen biosynthesis. In MCF-7shPRODH/POX clones, these processes, as well as energetic metabolism, were remarkably suppressed. The data for the first time suggest that celecoxib induces apoptosis through upregulation of PRODH/POX in MCF-7 breast cancer cells.

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Wang, Li-Ping, Zhi Xu, Gui-Ying Deng, and Sha-Li Xu. "Antiproliferative Activity of 8-methoxy Ciprofloxacin-Hydrozone/Acylhydrazone Scaffolds." Current Topics in Medicinal Chemistry 20, no. 21 (September 18, 2020): 1911–15. http://dx.doi.org/10.2174/1568026620666200603105644.

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Aims: A series of 8-methoxy ciprofloxacin- hydrazone/acylhydrazone hybrids were evaluated for their activity against a panel of cancer cell lines including HepG2 liver cancer cells, MCF-7, doxorubicin- resistant MCF-7 (MCF-7/DOX) breast cancer cells, DU-145 and multidrug-resistant DU145 (MDR DU-145) prostate cancer cells to seek for novel anticancer agents. Background: Ciprofloxacin with excellent pharmacokinetic properties as well as few side effects, is one of the most common used antibacterial agents. Notably, Ciprofloxacin could induce cancer cells apoptosis, and cell cycle arrest at the S/G2 stage. The structure-activity relationship reveals that the introduction of the methoxy group into the C-8 position of the fluoroquinolone moiety has resulted in a greater binding affinity to the binding site, and 8-methoxy ciprofloxacin derivatives have proved a variety of biological activities even against drug-resistant organisms. However, to the best of our current knowledge, there are no studies that have reported the anticancer activity of 8-methoxy ciprofloxacin derivatives so far. Furthermore, many fluoroquinolone-hydrazone/acylhydrazone hybrids possess promising anticancer activity. Thus, it is rational to screen the anticancer activity of 8-methoxy ciprofloxacin derivatives. Objective: To enrich the structure-activity relationship and provide new anticancer candidates for further investigations. Methods: The desired 8-methoxy ciprofloxacin-hydrazone/acylhydrazone hybrids 5 and 6 were screened for their in vitro anticancer activity against liver cancer cells HepG2, breast cancer cells MCF-7, MCF7/DOX, prostate cancer cells DU-145 and MDR DU-145 by MTT assay. Results: Some of 8-methoxy ciprofloxacin-hydrazone hybrids showed potential activity against HepG2, MCF-7, MCF-7/DOX, DU-145 and MDR DU-145 cancer cell lines, low cytotoxicity towards VERO cells and promising inhibitory activity on tubulin polymerization. Conclusion: Compounds 5d and 5f showed promising anticancer activity, low cytotoxicity, and potential tubulin polymerization inhibitory activity, were worthy of investigation. Other: The structure-activity relationship was enriched.

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Nguyen, Oanh Thi-Kieu, Anh Nguyen Tu Bui, Ngoc Bich Vu, and Phuc Van Pham. "ID: 1077 Overexpress of CD47 does not alter stemness of MCF-7 breast cancer cells." Biomedical Research and Therapy 4, S (September 5, 2017): 163. http://dx.doi.org/10.15419/bmrat.v4is.351.

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Background: CD47 is a transmembrane glycoprotein expressed on all cells in the body and particularly overexpressed on cancer cells and cancer stem cells of both hematologic and solid malignancies. In the immune system, CD47 acts as a "don't eat me" signal, inhibiting phagocytosis by macrophages by interaction with signal regulatory protein α (SIRPα). In cancer, CD47 promotes tumor invasion and metastasis. This study aimed to evaluate the stemness of breast cancer cells when CD47 is overexpressed. Methods: MCF-7 breast cancer cells were transfected with plasmid pcDNA3.4-CD47 containing the CD47 gene. The stemness of the transduced MCF7 cell population was evaluated by expression of CD44 and CD24 markers, anti-tumor drug resistance and mammosphere formation Results: Transfection of plasmid pcDNA3.4-CD47 significantly increased the expression of CD47 in MCF-7 cells. The overexpression of CD47 in transfected MCF-7 cells led to a significant increase in the CD44+CD24- population, but did not increase doxorubicin resistance of the cells or their capacity to form mammospheres. Conclusion: CD47 overexpression enhances the CD44+CD24- phenotype of breast cancer cells as observed by an increase in the CD44+CD24- expressing population. However, these changes are insufficient to increase the stemness of breast cancer cells.

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van Deurs, B., Z. Z. Zou, P. Briand, Y. Balslev, and O. W. Petersen. "Epithelial membrane polarity: a stable, differentiated feature of an established human breast carcinoma cell line MCF-7." Journal of Histochemistry & Cytochemistry 35, no. 4 (April 1987): 461–69. http://dx.doi.org/10.1177/35.4.3546491.

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Carcinoma cells typically show little or no polarity as compared to normal, differentiated epithelial cells. We have studied polarity in two established human breast carcinoma cell lines, T47D and MCF-7, by various techniques (electron microscopic enzyme- and immunocytochemistry, freeze-fracture) and show that one of them (MCF-7) is characterized by a high degree of polarity. Thus, in contrast to T47D cells, MCF-7 cells in monolayer culture form apical tight junctions, do not allow a ricin-horseradish peroxidase conjugate, which binds to terminal galactose residues on the apical surface, to stain the basolateral membrane domain, and express a surface antigen (MFGM-A) only in the apical surface membrane domain, as do normal mammary epithelial cells in vivo. This polarization is independent of a basement membrane, since it is maintained when MCF-7 cells, which do not deposit type IV collagen themselves, are grown directly on plastic. Moreover, even though MCF-7 cells express estrogen receptors rather homogeneously, estrogen has no effect on this polarity, neither in vitro nor after transplantation to nude mice. We conclude that polarity is a stable, differentiated feature of MCF-7 cells.

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Chekhun, V. F., I. V. Zalutskii, L. A. Naleskina, N. Yu Lukianova, T. M. Yalovenko, T. Borikun, S. O. Sobchenko, I. V. Semak, and V. S. Lukashevich. "MODIFYING EFFECTS OF LACTOFERRIN IN VITRO ON MOLECULAR PHENOTYPE OF HUMAN BREAST CANCER CELLS." Experimental Oncology 37, no. 3 (September 22, 2015): 181–86. http://dx.doi.org/10.31768/2312-8852.2015.37(3):181-186.

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Aim: To assess the role of endogenous lactoferrin (LF) in the formation of the molecular phenotype of human breast cancer (BC) cell lines with varying degrees of malignancy, including cisplatin/doxorubicin resistant cell lines, and identify possible impact of exogenous LF. Materials and Methods: 5 breast cell lines of different origin — MCF-10 A, MCF-7, including doxorubicin/ cisplatin resistant ones, T47D, MDA-MB-231, and MDA-MB-468. Immunocytochemistry: e xpression of LF, Ki-67, adhesion molecules E- and N-cadherin, CD44, CD24 rating the invasive potential of cells. Results: Expression of LF in human BC cell lines varies. It is associated with the heterogeneity of molecular profiles of cell lines in terms of adhesion. A link has been established between the level of LF expression in the resistant cell line MCF-7/CP and MCF-7/Dox, features of their molecular profile and invasive properties. Exogenous LF was shown to be capable of modifying the molecular profile and invasive properties of all the studied cell lines including resistant ones (MCF-7/CP and MCF-7/Dox). Conclusions: The sensitivity of cytostatic-resistant cell lines (MCF-7/CP and MCF-7/Dox) tends to increase under the influence of exogenous LF. It is likely that this effect is due to LF-mediated inhibition of the expression of proteins associated with drug resistance.

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Tan, Aik-Aun, Wai-Mei Phang, Subash C. B. Gopinath, Onn H. Hashim, Lik Voon Kiew, and Yeng Chen. "Revealing Glycoproteins in the Secretome of MCF-7 Human Breast Cancer Cells." BioMed Research International 2015 (2015): 1–8. http://dx.doi.org/10.1155/2015/453289.

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Breast cancer is one of the major issues in the field of oncology, reported with a higher prevalence rate in women worldwide. In attempt to reveal the potential biomarkers for breast cancer, the findings of differentially glycosylated haptoglobin and osteonectin in previous study have drawn our attention towards glycoproteins of secretome from the MCF-7 cancer cell line. In the present study, further analyses were performed on the medium of MCF-7 cells by subjecting it to two-dimensional analyses followed by image analysis in contrast to the medium of human mammary epithelial cells (HMEpC) as a negative control. Carboxypeptidase A4 (CPA4), alpha-1-antitrypsin (AAT), haptoglobin (HP), and HSC70 were detected in the medium of MCF-7, while only CPA4 and osteonectin (ON) were detected in HMEpC medium. In addition, CPA4 was detected as upregulated in the MCF-7 medium. Further analysis by lectin showed that CPA4, AAT, HP, and HSC70 were secreted as N-glycan in the medium of MCF-7, with HP also showing differentially N-glycosylated isoforms. For the HMEpC, only CPA4 was detected as N-glycan. No O-glycan was detected in the medium of HMEpC but MCF-7 expressed O-glycosylated CPA4 and HSC70. All these revealed that glycoproteins could be used as glycan-based biomarkers for the prognosis of breast cancer.

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Zhang, Jun, He-da Zhang, Yu-Feng Yao, Shan-Liang Zhong, Jian Hua Zhao, and Jin Hai Tang. "β-Elemene Reverses Chemoresistance of Breast Cancer Cells by Reducing Resistance Transmission via Exosomes." Cellular Physiology and Biochemistry 36, no. 6 (2015): 2274–86. http://dx.doi.org/10.1159/000430191.

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Background: Currently, exosomes that act as mediators of intercellular communication are being researched extensively. Our previous studies confirmed that these exosomes contain microRNAs (miRNAs) that could alter chemo-susceptibility, which is partly attributed to the successful intercellular transfer of multidrug resistance (MDR)-specific miRNAs. We also confirmed that β-elemene could influence MDR-related miRNA expression and regulate the expression of the target genes PTEN and Pgp, which may lead to the reversal of the chemoresistant breast cancer (BCA) cells. We are the first to report these findings, and we propose the following logical hypothesis: β-elemene can mediate MDR-related miRNA expression in cells, thereby affecting the exosome contents, reducing chemoresistance transmission via exosomes, and reversing the drug resistance of breast cancer cells. Methods: MTT-cytotoxic, miRNA microarray, real-time quantitative PCR, Dual Luciferase Activity Assay, and Western blot analysis were performed to investigate the impact of β-elemene on the expression of chemoresistance specific miRNA and PTEN as well as Pgp in chemoresistant BCA exosomes. Results: Drug resistance can be reversed by β-elemene related to exosomes. There were 104 differentially expressed miRNAs in the exosomes of two chemoresistant BCA cells: adriacin (Adr) - resistant MCF-7 cells (MCF-7/Adr) and docetaxel (Doc) - resistant MCF-7 cells (MCF-7/Doc) that underwent treatment. Of these, 31 miRNAs were correlated with the constant changes in the MDR. The expression of miR-34a and miR-452 can lead to changes in the characteristics of two chemoresistant BCA exosomes: MCF-7/Adr exosomes (A/exo) and MCF-7/Doc exosomes (D/exo). The PTEN expression affected by β-elemene was significantly increased, and the Pgp expression affected by β-elemene was significantly decreased in both cells and exosomes. β-elemene induced a significant increase in the apoptosis rate in both MCF-7/Doc and MCF-7/Adr cells. Conclusions: Drug resistance can be reversed by β-elemene, which can alter the expression of some MDR-related miRNAs, including PTEN and Pgp in MCF-7/Adr and MCF-7/Doc in cells. It can therefore affect the exosome contents and induce the reduction of resistance transmission via exosomes.

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Welsh, JoEllen. "Induction of apoptosis in breast cancer cells in response to vitamin D and antiestrogens." Biochemistry and Cell Biology 72, no. 11-12 (November 1, 1994): 537–45. http://dx.doi.org/10.1139/o94-072.

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1,25-Dihydroxycholecalciferol D3 (1,25(OH)2D3), the active metabolite of vitamin D, is a potent inhibitor of breast cancer cell growth both in vivo and in vitro. We have shown that MCF-7 cells treated with 100 nM 1,25(OH)2D3 exhibit characteristic apoptotic morphology (pyknotic nuclei, chromatin and cytoplasmic condensation, nuclear matrix protein reorganization) within 48 h. In the experiments reported here, we examined the interactions between 1,25(OH)2D3 and the antiestrogen 4-hydroxytamoxifen (TAM), which also induces apoptosis in MCF-7 cells. Our data suggest that TAM significantly potentiates the reduction in cell number induced by 1,25(OH)2D3 alone. Combined treatment with 1,25(OH)2D3 and TAM enhances the degree of apoptosis assessed using morphological markers that identify chromatin and nuclear matrix protein condensation. We have selected a subclone of MCF-7 cells resistant to 1,25(OH)2D3 (MCF-7D3Res). These cells express the vitamin D receptor and exhibit doubling times comparable to the parental MCF-7 cells, even when grown in 100 mM 1,25(OH)2D3. Treatment of both parental and resistant MCF-7 cells with TAM induces apoptosis and clusterin. These data emphasize that apoptosis can be induced in MCF-7 cells either by activation of vitamin-D-mediated signalling or disruption of estrogen-dependent signalling.Key words: apoptosis, breast, vitamin D, antiestrogen, gene expression, clusterin.

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Pottle, Jonathan, Chengrong Sun, Lloyd Gray, and Ming Li. "Exploiting MCF-7 Cells’ Calcium Dependence with Interlaced Therapy." Journal of Cancer Therapy 04, no. 07 (2013): 32–40. http://dx.doi.org/10.4236/jct.2013.47a006.

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Journal articles on the topic 'MCF-7 cells'

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