Double-stranded RNA-specific adenosine deaminase-knockdown inhibits the proliferation and induces apoptosis of DU145 and PC3 cells by promoting the phosphorylation of H2A.X variant histone.

Double-stranded RNA-specific adenosine deaminase (ADAR1) is a member of the adenosine deaminases acting on RNA family that catalyze the adenosine-to-inosine editing of double-stranded RNA substrates. Several studies have reported that ADAR1 is closely associated with numerous malignancies. However, the functional roles of ADAR1 in prostate cancer (PCa) have not been fully elucidated. Thus, the present study aimed to investigate the effects of ADAR1 on PCa. The results demonstrated that ADAR1 was highly expressed in PCa tissues compared with normal tissues. Furthermore, the protein expression level of ADAR1 was significantly increased in castration-resistant PCa (CRPCa) tissues and CRPCa cell lines. Thus, these findings indicated that ADAR1 may act as a tumor promoter for PCa development. Next, the potential effects of ADAR1-knockdown on the proliferation of DU145 and PC3 cells were investigated. ADAR1 was knocked down via small interfering RNA transfection, which was found to exert antitumor effects on DU145 and PC3 cells at 24 and 48 h post transfection. Furthermore, a significant positive association was observed between ADAR1-knockdown and the apoptosis of DU145 and PC3 cells, which increased the phosphorylation of H2A.X variant histone. The results of the present study indicated a positive association between ADAR1 expression and PCa, which may promote the development of CRPCa. Moreover, ADAR1-knockdown may serve as a tumor suppressor and represent a potential target for the treatment of PCa.