Immature Colon Carcinoma Transcript 1 Is Essential for Prostate Cancer Cell Viability and Proliferation.
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...
| Publicado en: | Cancer Biotherapy & Radiopharmaceuticals Vol. 30; no. 7; pp. 278 - 285 |
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| Autores principales: | , , , , , , , , , |
| Formato: | corrected article Journal Article |
| Publicado: |
Mary Ann Liebert, Inc.
Sep2015
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| Acceso en línea: | Ver este registro en EBSCOhost |
| fields | @attributes: recordID: 1 pdfLink: plink: https://search.ebscohost.com/login.aspx?direct=true&db=ccm&AN=109646761&site=ehost-live header: @attributes: shortDbName: ccm uiTerm: 109646761 longDbName: CINAHL Complete uiTag: AN controlInfo: bkinfo: dissinfo: jinfo: jid: 10849785 N3A jtl: Cancer Biotherapy & Radiopharmaceuticals issn: 10849785 maglogo: N pubinfo: dt: Sep2015 vid: 30 iid: 7 pid: 1365 pub: Mary Ann Liebert, Inc. place: New Rochelle, New York artinfo: ui: 109646761 109646761 NLM26186090 2013165158 10.1089/cbr.2014.1728 NLM26186090 109646761 ppf: 278 ppct: 7 formats: tig: atl: Immature Colon Carcinoma Transcript 1 Is Essential for Prostate Cancer Cell Viability and Proliferation. aug: au: Wang, Zhijun Xu, Danfeng Gao, Yi Liu, Yushan Ren, Jizhong Yao, Yacheng Yin, Lei Chen, Jie Gan, Sishun Cui, Xingang sug: ab: 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. pubtype: Academic Journal doctype: corrected article Journal Article ougenre: Article language: English refInfo: holdings: @attributes: islocal: N |
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