Bladder polypoid cystitis-derived A20 associates with tumorigenesis.

Bladder chronic inflammation is associated with the pathogenesis of bladder cancer; the underlying mechanism is unclear. The PT53 gene is an important anticancer gene in the body, which is suppressed in cancer. The ubiquitin E3 ligase A20 (A20) plays a role in regulating the activities of epithelial cells. This study was designed to investigate the correlation between A20 and the pathogenesis of bladder cancer. The biopsy tissues of human bladder cancer, bladder polypoid cystitis, and chronic inflammation were collected; the levels of A20 and p53 were analyzed by quantitative real-time RT-PCR, Western blotting, and immune precipitation. HEK293 cells were employed to test the role of overexpression of A20 in the suppression of the p53 gene in the cells. Fifty-six patients with bladder cancer, 48 patients with bladder polypoid cystitis, and 16 patients with bladder chronic inflammation were recruited into this study. Human bladder cancer tissue and the polypoid tissue showed high levels of A20, which had a positive correlation with the tumorigenesis in the bladder; 12 out of 46 (26.1%) patients with bladder polypoid cystitis were diagnosed as bladder cancer. A20 bound to p53 to form complexes in bladder cancer tissue and bladder polypoid tissue. The overexpression of A20 suppresses p53 protein levels in HEK293 cells. A20 has a positive correlation in the tumorigenesis of bladder polypoid disorders.