MicroRNA-107 inhibits proliferation of prostate cancer cells by targeting cyclin E1.

Previous studies have reported that miR-107 could be utilized as a potential peripheral biomarker in prostate cancer (PCa). However, the specific functions of miR-107 in prostate cancer and its relevant mechanisms are still unknown. The aim of this research was to investigate the cellular functions of miR-107 in PCa and reveal the relevant mechanisms. MicroRNA tailing quantitative real-time PCR (qRT-PCR) was adopted to measure the expression of miR-107 in PCa cell line DU145 and PC3, as well as in normal prostate cell line RWPE-1. The miR-107 expression pattern in PCa tissues and paired peritumoral tissues were determined by Chromogenic In Situ Hybridization (CISH). Cell viability, colony formation, flow cytometry cell cycle and apoptosis, wound healing and Transwell migration assays were performed to study the miR-107 functions in PCa cells. Further, qRT-PCR, western blot analysis and dual-luciferase reporter assays were conducted to verify the target of miR-107 in PCa. Results demonstrated that miR-107 was downregulated in PCa cells and tissues in comparison with normal prostate cells and peritumoral tissues, and the over-expression of miR-107 suppressed proliferation and induced G1/S arrest of PCa cells but had no effects on apoptosis or cell motility of PCa cells. MiR-107 was found to target cyclin E1 (CCNE1) in PCa cells by directly binding to its 3'-UTR. In conclusion, miR-107 could be a potential tumor suppressor in PCa, and the restoration of miR-107 might provide a new therapeutic option for PCa.