MiR-1 inhibits prostate cancer PC3 cells proliferation through the Akt/mTOR signaling pathway by binding to c-Met.

Prostate cancer (PC) is known as the most common cancer and is ranked second in cancer-related deaths in males. Accumulating evidence implicates microRNAs (miRNAs) may play key roles in tumorigenesis. We investigated the effects of microRNA-1 (miR-1) on the viability and proliferation of prostate cancer cells and the underlying mechanism. We first detected the miR-1 expression level in the PC cells by quantitative real-time PCR (qRT-PCR). The relation between the level of miR-1 and c-Met was investigated via luciferase reporter assay. Cell viability and proliferation were analyzed via MTT assay and flow cytometry in PC cells. Western blot was used for examining the related signaling pathway. MiR-1 expression was decreased and c-Met expression was increased in PC cells. Subsequently, we found that overexpression of miR-1 could inhibit viability and proliferation of PC cells functionally. Furthermore, the dual luciferase reporter assay results indicated that the c-Met is the target gene of miR-1. Western blot results indicated that this inhibition on the viability and proliferation of PC cells was via regulation of c-Met/AKT/mTOR signaling pathway. In conclusion, this study provides novel insight into the role of miR-1 in PC, and the results demonstrated that miR-1 could inhibit viability and proliferation of PC cells by targeting the c-Met/Akt/mTOR signaling pathway. MiR-1 might be a potential candidate for application in the treatment of PC.

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