Objective: To systematically investigate the expression of mi R-1 in renal cell carcinoma(RCC) tissues and RCC cell lines. To investigate the mi R-1-mediated inhibition of cell cycle progression. To explore the function and molecular mechanism of mi R-1 during proliferation, migration and invasion of RCC.Method:The expression of mi R-1 in RCC cell lines and renal tissues were measured by q RT-PCR. Colony-forming Assay, MTS,Ed U assay were performed to detect the proliferation ability of mi R-1.The cell cycle progression was detected by flow cytometry technique. Transwell assay were performed to detect the migration and invasion ability of mi R-1. The western blot and luciferase reporter assay were performed to detect the direct targeting genes of mi R-1.Results: In contrast of normal tissues and renal cell lines, the expression of mi R-1 in renal cancer cell lines and renal cancer tissues had a significantly lower expression with a P value less than 0.05. Gain of function assay have showed that mi R-1 mimics can inhibit the proliferation migration and invasion ability. Conversely, Loss of function assay demonstrated mi R-1 inhibitor promoted cell proliferation and metastasis in RCC. The flow cytometry results unveiled that renal cancer cells transfected with mi R-1 displayed a significant increase in the percentages of cells in G1 phase. The luciferase reporter assay and western blot showed that CDK4, CDK6, Caprin1 and Slug are direct targets of mi R-1.Conclusion: As a tumor suppressor gene, mi R-1 played a significant role in the suppression of tumorigenesis and development of RCC and mi R-1 can serve as a potential target for therapy of RCC. |