AB060. Lost expression of cell adhesion molecule 1 (CADM1) associated with bladder cancer progression and recurrence and its overexpression inhibited tumor cell malignant behaviors

OBJECTIVE: To investigate the function of CADM1 in bladder cancer malignant behaviors METHODS: This study assessed CADM1 expression in 84 cases of bladder tissues for association with clinicopathological parameters from bladder cancer patients and then investigated the effects of CADM1 overexpression on bladder cancer cells in vitro. RESULTS: Expression of CADM1 protein was significantly reduced in bladder cancer tissues (0.26±0.14) than in normal bladder mucosa (0.69±0.092; P<0.01), and methylation of CADM1 promoter was responsible for silence of CADM1 protein expression and significantly associated with tumor size, recurrence, pathology classification, and clinical stage (P<0.05). Overexpression of CADM1 protein inhibited tumor cell proliferation, but reduced tumor cell invasion capacity and induced tumor cell apoptosis in vitro. At the gene level, CADM1 expression upregulated caspase-3 activity and expression of Bax and p27 protein and downregulated levels of bcl-2, cyclinD1, cyclinE1, and CDK2 proteins. Moreover, overexpression of CADM1 regulated expression of epithelial to mesenchymal transition (EMT) markers, including increased expression of E-cadherin and β-catenin, whereas decreased the levels of Vimentin. CONCLUSIONS: This study demonstrated that lost expression of CADM1 protein could exert an essential role in development and progression of bladder cancer and suggests that CADM1 may be a novel molecular target for control of this disease in clinic.