MiR-22 suppresses the growth and metastasis of bladder cancer cells by targeting E2F3.

Bladder cancer is a common, serious disease worldwide. MicroRNAs (miRNAs) have been reported to participate in the development and progression in many cancers, including bladder cancer. However, the exact roles of miR-22 in bladder cancer process and its underlying mechanism remain largely unknown. The expression levels of miR-22 and E2F3 were analyzed by quantitative real-time polymerase chain reaction (qRT-PCR). Western blot was used to detect the protein levels of E2F3, E-cadherin, N-cadherin, and Vimentin in bladder cancer cells. Cell viability, proliferation, migration, and invasion were determined by 3-(4,5-dimethylthiazol-2-yl)-2,5 diphenyltetrazolium bromide (MTT) assay, colony formation assay, and transwell assay, respectively. The potential binding sites between miR-22 and E2F3 were predicted by TargetScan and verified by luciferase report assay. The expression of miR-22 was downregulated and E2F3 expression was upregulated in bladder cancer tissues and cells. Overexpression of miR-22 or E2F3 knockdown inhibited cell proliferation, migration, invasion, and epithelial-mesenchymal transition (EMT) in bladder cancer cells. In addition, E2F3 was a direct target of miR-22 and its knockdown attenuated the promotion of cell proliferation, migration, invasion, and EMT induced by miR-22 inhibitor in bladder cancer cells. In conclusion, miR-22 suppressed cell proliferation, migration, invasion, and EMT in bladder cancer cells by regulating E2F3 expression, providing a novel avenue for treatment of bladder cancer. IJCEP