Objective      To determine the role and underlying mechanism of miR-200c in the proliferation of bladder cancer.       Methods      After lentiviruses were used to stably over-express and antagonize miR-200c in bladder cancer 5637

TCC-SUP and UM-UC-3 cells

RT-qPCR and Western blotting were intended to detect the expression changes of miR-200c and KRAS. Dual luciferase reporting system was used to verify whether miR-200c regulated the 3′UTR of KRAS as target. Colony formation assay was applied to analyze the change of colony formation abilities of bladder cancer cells in different groups.       Results      CCK-8 assay that cell viability was 0.833 3±0.062 1 and 0.650 3±0.088 7 in the controlled and miR-200c T24 cells (P0.05)

and 0.939 0±0.018 1 and 0.806 0±0.021 6 in the controlled and miR-200c UM-UC-3 cells (P0.01). Stably over-expression of miR-200c resulted in significant decrease in protein expression of KRAS (P0.05).       Conclusion      miR-200c suppresses the proliferation of bladder cancer cells by down-regulating the expression of KRAS protein

which indicates that KRAS plays a vital role in the incidence and progression of bladder cancer.