[miR-153-3p inhibits proliferation and migration of breast cancer cells via down-regulating ROCK1].

Objective To investigate the molecular mechanism of miR-153-3p regulating the proliferation, migration and invasion of human breast cancer cells. Methods Bioinformatics software was used to predict the candidate target gene of miR-153-3p. The double-luciferase reporter assay was used to validate the targeting relationship between miR-153-3p and candidate genes. Real-time fluorescence quantitative PCR and Western blotting were performed to detect the effect of miR-153-3p on the mRNA and protein expressions, respectively. The cell proliferation ability was examined by MTT assay. The migration ability of cells was determined in a scratch assay. The invasion ability was detected by TranswellTM assay. Results Software-predicted results showed a continuous binding region between miR-153-3p and Rho-associated coiled-coil containing protein kinase 1 (ROCK1). The miR-153-3p mimics co-transfected with ROCK1 wild-type reporter vector significantly decreased the relative activity of luciferase in MDA-MB-231 cells. The transfection of hsa-miR-153-3p mimics increased miR-153-3p expression and decreased ROCK1 protein expression. In comparison with the control cells, the proliferation, migration and invasion of MDA-MB-231 cells over-expressing miR-153-3p were dramatically inhibited. Conclusion The miR-153-3p can inhibit the proliferation, migration and invasion of breast cancer cells via down-regulation of ROCK1.