MiR-129 inhibits breast cancer cell proliferation, migration and invasion by targeting CAMK2N1

Abstract

Objective To investigate the role and potential mechanism of microRNA-129(miR-129) in the progress of proliferation, apoptosis and migration in breast cancer. Methods The expression of miR-129 in three breast cancer cell lines (MCF-7, MDA-MB-231, T47D) and one normal breast epithelial cell line (MCF-10A) was detected by real-time fluorescence quantitative reverse transcription PCR(qRT-PCR). Cell colony formation and cell counting kit-8 (CCK-8) were used to characterize the role of miR-129 in the proliferation of breast cancer.Wound healing and transwell were used to test the migration of miR-129 in breast cancer.A miR-129 target gene was identified with Western blot and luciferase activity assays. Results Compared with normal mammary epithelial cell MCF-10A, miR-129 was down-regulated in vitro cell lines (MCF-10A: 1.21±0.3, MCF-7: 0.52±0.2, MDA-MB-231: 0.43±0.1, T47D: 0.82±0.24; t values were 4.02, 4.23 and 3.87 respectively, all P values<0.05). Up-regulation of miR-129 can significantly inhibit the activity of breast cancer MCF-7 cells(t=4.14, P<0.05). Over-expression of miR-129 could significantly inhibit the proliferation of MCF-7 cells (miR-129 inhibitor: 52±18; t=4.24, P<0.05). Otherwise, miR-129 inhibitor could promote the proliferation of MCF-7 cells(miR-129 mimic: 156±12; t=4.13, P<0.05)and also significantly inhibit the invasion and migration of MCF-7 cells.In addition, CAMK2N1 has been proved to be a direct target of miR-129. Conclusion The miR-129 can act as a tumor suppressor and regulate the progression of breast cancer by targeting CAMK2N1. Key words: Breast cancer; miR-129; CAMK2N1; Proliferation; Migration