Abstract
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.