MiR-26a inhibits cell proliferation and induces apoptosis in human bladder cancer through regulating EZH2 bioactivity.

Bladder cancer is the second most common malignant tumor of the urinary tract worldwide and is associated with significant morbidity and mortality. EZH2, the enzymatic subunit of Polycomb repressive complex 2 (PRC2), is frequently overexpressed in multiple tumor types including Bladder cancer and plays multiple roles in tumor cell proliferation and apoptosis. Previous study showed that miR-26a has different roles in different tumors and the expression of EZH2 is identified as a potential target of miR-26a which miR-26a has been found to decrease in bladder cancer. But the mechanism between EZH2 and miR-26a is not completely clear in bladder cancer. Western blot and Real-time PCR were involved to detect both expression of mRNA and protein of EZH2. And we used mimics-miR26a to elaborate the relationship between EZH2 and miR-26a in cell proliferation and apoptosis process through lots of specific assays. The results showed that EZH2 express mainly in bladder tumor tissues than para-carcinoma tissues. Meanwhile, miR26a can down-regulate the expression of EZH2 through suppressing EZH2 activity. Both miR26a and downregulated EZH2 can induce bladder cancer cell apoptosis and increase cell at G1 stage as well as suppress cell proliferation. The further assays reveal that miR-26a can suppress cell proliferation and enhance cell apoptosis through EZH2. In this study, we found that EZH2 was overexpressed in bladder tumor tissue and miR-26a could downregulate the expression of EZH2 to inhibit proliferation and enhance apoptosis in bladder cancer.