title: Immature Colon Carcinoma Transcript 1 Is Essential for Prostate Cancer Cell Viability and Proliferation.
abstract: 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.
authors.affiliation: Department of Urology, Changzheng Hospital, The Second Military Medical University , Shanghai, China .
authors.forename: Zhijun
authors.initials: Z
authors.lastname: Wang
authors.affiliation: Department of Urology, Changzheng Hospital, The Second Military Medical University , Shanghai, China .
authors.forename: Danfeng
authors.initials: D
authors.lastname: Xu
authors.affiliation: Department of Urology, Changzheng Hospital, The Second Military Medical University , Shanghai, China .
authors.forename: Yi
authors.initials: Y
authors.lastname: Gao
authors.affiliation: Department of Urology, Changzheng Hospital, The Second Military Medical University , Shanghai, China .
authors.forename: Yushan
authors.initials: Y
authors.lastname: Liu
authors.affiliation: Department of Urology, Changzheng Hospital, The Second Military Medical University , Shanghai, China .
authors.forename: Jizhong
authors.initials: J
authors.lastname: Ren
authors.affiliation: Department of Urology, Changzheng Hospital, The Second Military Medical University , Shanghai, China .
authors.forename: Yacheng
authors.initials: Y
authors.lastname: Yao
authors.affiliation: Department of Urology, Changzheng Hospital, The Second Military Medical University , Shanghai, China .
authors.forename: Lei
authors.initials: L
authors.lastname: Yin
authors.affiliation: Department of Urology, Changzheng Hospital, The Second Military Medical University , Shanghai, China .
authors.forename: Jie
authors.initials: J
authors.lastname: Chen
authors.affiliation: Department of Urology, Changzheng Hospital, The Second Military Medical University , Shanghai, China .
authors.forename: Sishun
authors.initials: S
authors.lastname: Gan
authors.affiliation: Department of Urology, Changzheng Hospital, The Second Military Medical University , Shanghai, China .
authors.forename: Xingang
authors.initials: X
authors.lastname: Cui
mesh_terms: D002453:Cell Cycle / Q000235:genetics; D045744:Cell Line, Tumor; D049109:Cell Proliferation / Q000502:physiology; D002470:Cell Survival / Q000502:physiology; D015536:Down-Regulation; D055785:Gene Knockdown Techniques; D057809:HEK293 Cells; D006801:Humans; D008297:Male; D011471:Prostatic Neoplasms / Q000235:genetics* / Q000378:metabolism / Q000473:pathology*; D011506:Proteins / Q000235:genetics* / Q000378:metabolism*; D012269:Ribosomal Proteins
chemical_list: C098021:MRPL58 protein, human; D011506:Proteins; D012269:Ribosomal Proteins
keywords: ICT1; apoptosis; proliferation; prostate cancer; shRNA