Prostate cancer is the second leading cause of cancer-related death among men in the United States. More recently, immature colon carcinoma transcript 1 (ICT1) has been reported to be overexpressed in various kinds of cancer cells. However, the role of ICT1 in human prostate cancer has not yet been determined. The authors selected two ICT1-specific short hairpin RNA (shRNA) sequences to block its endogenous expression in human androgen-independent prostate cancer cell lines DU145 and PC-3. Decreased ICT1 expression by either specific shRNA significantly inhibited cell viability and proliferation. Moreover, compared to controls, ICT1-silenced cells were more inclined to redistribute in the G2/M phase, leading to cell cycle arrest. Flow cytometry and Annexin V-APC/7-AAD double staining confirmed that knockdown of ICT1 increased late apoptotic cells. Furthermore, they found that ICT1 knockdown restricting G2-M transition may be partly through suppression of CDK1 and Cyclin B1. Knockdown of ICT1 induced apoptosis through activation of poly ADP-ribose polymerase and caspase 3, upregulation of Bax expression, and downregulation of Bcl-2 expression in DU145 cells. In conclusion, this study highlights the crucial role of ICT1 in promoting prostate cancer cell proliferation in vitro. The depletion of ICT1 by lentivirus-mediated shRNA or small molecular inhibitor may provide a novel therapeutic approach for the treatment of prostate cancer.
Keywords: ICT1; apoptosis; proliferation; prostate cancer; shRNA.