ECT 2 gene-silencing regulates the proliferation and apoptosis of human breast cancer cells and its mechanism / 肿瘤

ABSTRACT

Objective: To investigate the effects of epithelial cell transformingsequence 2 oncogene (ECT 2) gene-silencing on the proliferation and apoptosis of human breast cancer cells, as well as its potential molecular mechanism. Methods: Firstly, the expressions of ECT2 mRNA and protein in normal mammary epithelial cells (MCF-10A) and breast cancer cells (MDA-MB-231, SK-BR-3, MCF-7, and BT474) were detected by real-Time fluorescent quantitative PCR and Western blotting, respectively. After transfection with the specific siRNA targeting ECT 2 gene (ECT2 siRNA) and treatment with extracellular regulated protein kinase (ERK) pathway activator or transfection with microRNA-101 (miR-101) inhibitor, the proliferation and apoptosis of MDA-MB-231 and MCF-7 cells were detected by CCK-8 and FCM assay, respectively. Then the levels of phospho-ERK (p-ERK), Ras-related C3 botulinum toxin substrate 1 (Rac1) and miR-101 in MDA-MB-231 and MCF-7 cells were detected by Western blotting and real-Time fluorescent quantitative PCR. Results: The expression levels of ECT2 mRNA and protein in breast cancer cells were significantly increased as compared with those in normal mammary epithelial cells (both P 0.05). Conclusion: ECT 2 gene-silencing may affect the proliferation and apoptosis of breast cancer cells by ERK-miR-101-Rac1 signaling pathway.