Effect of miR-7 on resistance of breast cancer cells to adriamycin via regulating EGFR/PI3K signaling pathway

Q. Huang, Y.-Y. Wu, S.-J. Xing, Z.-W. Yu

Department of Pharmacy, Affiliated Xiaolan Hospital of Southern Medical University, Zhongshan, China. zewooyu@gzhmu.edu.cn

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• Oncology

OBJECTIVE: To explore whether micro ribonucleic acid (miR)-7 affects the resistance of breast cancer cells to adriamycin (ADR) through regulating the epidermal growth factor receptor (EGFR)/phosphatidylinositol 3-hydroxy kinase (PI3K) signaling pathway.
MATERIALS AND METHODS: MiR-7 expression was compared among MCF-10A, MCF-7 and MCF-7/ADR cells. The MCF-7/ADR cells were divided into three groups, namely miR-7 control group (MCF-7/ADR drug-resistant strains), miR-7 inhibition group (miR-7-inhibited MCF-7/ADR drug-resistant strains) and miR-7 promotion group (MCF-7/ADR drug-resistant strains transfected with miR-7), and the messenger RNA (mRNA) and protein expression levels of MCF-7/ADR were evaluated via Western blotting.
RESULTS: The expression level of miR-7 was substantially decreased in MCF-7 and MCF-7/ADR cells (p<0.05), and it was lowered more obviously in MCF-7/ADR cells than that in MCF-7 cells (p<0.05). Compared with that in miR-7 control group, miR-7 expression in miR-7 promotion group was notably raised (p<0.05), proving that the sensitivity of MCF-7/ADR cells to ADR was enhanced, while that in miR-7 inhibition group was significantly lowered (p<0.05). Compared with those in miR-7 control group, the mRNA and protein expression levels of EGFR and PI3K were elevated in miR-7 inhibition group (p<0.05), while they were lowered in miR-7 promotion group (p<0.05). Additionally, compared with those in miR-7 control group, the proliferation and apoptosis abilities of cells in miR-7 inhibition group were markedly enhanced (p<0.05) and weakened (p<0.05), respectively, while they were weakened (p<0.05) and significantly strengthened (p<0.05), respectively in miR-7 inhibition group.
CONCLUSIONS: MiR-7 plays an important role in the resistance of breast cancer cells to ADR, and its over-expression can inhibit the EGFR/PI3K signaling pathway to raise their sensitivity to the chemotherapy drug ADR.

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