Function of Cancer stem cells in drug resistance of ER+ breast Cancer

Journal of Molecular Cancer  gives dependable data upgrade to online viewers with the adapted methods and most advancement in the field of Clinical cancer medicine. The editor’s welcome articles of current interest on research across Molecular Cancer, Cell and Tumor Biology, Angiogenesis, Cancer Antigens, Cellular Signaling and Molecular Biology, Genetic And Molecular Profiling of Cancer, DNA Damage and Repair, Cell Cycle, Metastasis.

Breast cancer (BC) is classified into ER+ and ER− tumors based on Estrogen Receptor (ER) status. ER+ tumors exhibit higher levels of resistance to chemotherapy compared to ER− tumors. It was shown that BCL-2, TP53, BAX and NF-ΚB are involved in drug resistance in the ER+ tumors. Cancer Stem Cells (CSCs) were shown to be the origin of cancer and play an important role in drug resistance. Here we introduce a commentary on our previously published study entitled (“Estrogen Receptor positive breast tumors resist chemotherapy by the overexpression of P53 in Cancer Stem Cells”) where we tested the hypothesis that CSCs of the ER+ tumors resist drug through the overexpression of BCL-2, TP53, BAX and NF-ΚB. CSCs (untreated or treated with Doxorubicin (DOX)) were isolated from MCF7 (ER+) and MDA-MB-231 (ER−) cell lines. mRNA expression levels of BCL-2, TP53, BAX and NFKB were detected by quantitative real time PCR (qPCR) with and without treatment. Interestingly TP53 showed a striking increase in its expression in CSCs of the ER+ MCF7 cells compared to bulk cancer cells. In addition, TP53 showed exceptionally elevated level of mRNA expression in MCF7-CSCs compared to MDA-MB-231-CSCs. These results suggest that CSCs in the ER+ cells avoid the effect of drug treatment by increasing p53 expression.

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Regards,
Julia Gillard
Journal of Molecular Cancer
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