MicroRNA-195 inhibits epithelial-mesenchymal transition via downregulating CDK4 in bladder cancer.

Bladder cancer is one of the most common cancers in the world. Despite advanced development made to improve the diagnosis and therapy techniques for bladder cancer, patients always have a poor outcome based on its high potential for metastasis. MiR-195 was reported to have close relevance with the process of bladder cancer. However, the molecular mechanism of miR-195 underlying bladder cancer metastasis and epithelial-mesenchymal transition (EMT) remains unclear. The present study was done to explore the function of miR-195 on EMT and cell migration in bladder cancer. In the present study, we detected the level of miR-195 in 25 matched human bladder cancer tissues and normal adjacent tissues, as well as bladder cancer cell lines or normal cells. Additionally, we determined the effects of miR-195 on expression of CDK4, and the miR-195/CKD4 signaling cascade on cell cycle, invasion, migration, and viability. Results showed that miR-195 was down expressed in bladder cancer tissues and cell lines, which inhibited EMT, cell migration, and invasion. We identify CDK4, an early G1 cell cycle regulator, as a downstream target of miR-195. Also, we found that miR-195 could induce G1-phase arrest, inhibit cell invasion, migration, and viability through down-regulation of CDK4 expression in 5637 and BIU-87 cells. Our experimental data suggest an important role for miR-195/CDK4 in bladder tumorigenesis and provide a potential therapeutic strategy for bladder cancer.