Results showed that METTL3 promoted proliferation of bladder cancer cells both in vitro and in vivo by enhancing the binding of DGCR8 to pri-miRNA-221/222 through its m6A activity, which resulted in the accelerating maturation of pri-miR-221/222 and reduction of tumor suppressor PTEN, the target of miR-221 [59]. This evidence concerns the gene DGCR8 and urinary bladder cancer.