MiRNA-217 accelerates the proliferation and migration of bladder cancer via inhibiting KMT2D.

To uncover the biological function of miRNA-217 in the progression of bladder cancer and the underlying mechanism. Potential miRNAs binding KMT2D were predicted through online bioinformatics. Their expression levels in bladder cancer tissues and adjacent ones were determined. Through Pearson correlation analysis and survival analysis, the most potential miRNA candidate (miRNA-217) that targets and regulates KMT2D in bladder cancer was selected. Subsequently, expression levels of miRNA-217 and KMT2D in non-muscle invasive bladder cancer (NMIBC) and muscle invasive bladder cancer (MIBC) were detected. MiRNA-217 level in bladder cancer cell lines was determined as well. The interaction between KMT2D and miRNA-217 was verified by dual-luciferase reporter gene assay. Finally, regulatory effect of miRNA-217 on viability and migration in T24 and UMUC-3 cells were investigated. Five potential candidates that were upstream genes binding KMT2D were searched by bioinformatics. Among them, miRNA-217 was remarkably upregulated in bladder cancer tissues and closely linked to poor prognosis of affected patients. Moreover, dual-luciferase reporter gene assay verified the interaction between miRNA-217 and KMT2D. MiRNA-217 was able to downregulate mRNA and protein levels of KMT2D. Furthermore, knockdown of miRNA-217 attenuated viability and migration in bladder cancer cells. MiRNA-217 accelerates proliferative and migratory abilities in bladder cancer via inhibiting the level of tumor suppressor KMT2D, thereafter leading to the poor prognosis in bladder cancer patients.