Objective  To observe the effect of microRNA-186-5p（MiR-186-5p）on the invasion and proliferation of renal cancer cells in vitro and explore the possible mechanisms.   Methods  Culture normal renal tubular epithelial cell line HK-2, primary and MiR-186-5p-transfected renal cancer cells (Caki-2 cells). Real-time PCR was used to detect the level of MiR-186-5p, the cell counting kit-8 (CCK-8) method  was used to evaluate the survival rate of each group of cells, the Transwell method  was used to detect the cell migration and invasion ability, and Western blotting was used to detect phosphorylated protein kinase B (p-Akt) and phosphorylated mammalian rapamycin target protein (p-mTOR) levels.   Results  The renal tubular epithelial cell line HK-2 and MiR-186-5p transfected Caki-2 cells had significantly higher MiR-186-5p levels than Caki-2 cells (P<0.05). The survival rates of HK-2 cells and Caki-2 cells were close to 100%, while the survival rate of Caki-2 cells transfected with MiR-186-5p. was significantly reduced to 72.86% (P<0.05). Compared with the migration number of HK-2 cells, Caki-2 cells migrated more (P<0.05); MiR-186-5p transfected Caki-2 cells migrated less (P<0.05). Compared with the phosphorylation level of Akt and mTOR molecules in HK-2 cells, the phosphorylation level of Akt and mTOR molecules in Caki-2 cells was significantly increased (P<0.05); Caki-2 cells transfected with MiR-186-5p. The phosphorylation level of Akt and mTOR molecules decreased (P<0.05).   Conclusion  MiR-186-5p can effectively inhibit the invasion and proliferation of renal cancer cells, which may be closely related by inhibiting the activation of Akt/mTOR signaling pathway.