More and more studies have shown that lncRNAs play critical roles in various biological processes of bladder cancer, including proliferation, apoptosis, migration and cell cycle arrest. Long non-coding RNA linc00511 is one of the lncRNAs highly expressed in bladder cancer tissues and cells. However, little is known about the roles and mechanisms of linc00511 in bladder cancer. Here, we demonstrated that linc00511 was highly expressed in bladder cancer tissues and cells. Linc00511 knockdown could cause the cell proliferation suppression and cell cycle arrest, which was mediated by p18, p21, CDK4, cyclin D1 and phosphorylation Rb. Suppressed linc00511 could induce the apoptosis in T24 and BIU87 cells via activating the caspase pathway. Down-regulation oflinc00511 could also suppress the migration and invasion of T24 and BIU87 cells. In addition, we found that the expression of linc00511 was negatively correlated with that of miR-15a-3p in the clinical bladder cancer samples. Further mechanistic studies showed that linc00511 knockdown induced proliferation inhibition and apoptosis increase might be regulated through suppressing the activities of Wnt/beta-catenin signaling pathway. Thus, we revealed that knockdown of linc00511 suppressed the proliferation and promoted apoptosis of bladder cancer cells through suppressing the activities of Wnt/beta-catenin signaling pathway. Moreover, we suggested that linc00511 could be a potential therapeutic target and novel biomarker in bladder cancer.