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dc.contributor.authorPickard, MRen_US
dc.contributor.authorEdwards, SEen_US
dc.contributor.authorCooper, CSen_US
dc.contributor.authorWilliams, GTen_US
dc.date.accessioned2018-08-17T14:58:15Z
dc.date.issued2010-10-01en_US
dc.identifier14en_US
dc.identifier.citationPROSTATE, 2010, 70 pp. 1513 - 1523en_US
dc.identifier.issn0270-4137en_US
dc.identifier.urihttps://repository.icr.ac.uk/handle/internal/2355
dc.identifier.doi10.1002/pros.21186en_US
dc.description.abstractBACKGROUND. The molecular control of cell death through apoptosis is compromised in prostate cancer cells, resulting in inappropriate cell survival and resistance to cytotoxic therapy. Reduced expression of the functionally connected apoptosis-regulators and candidate tumor suppressors Fau and Bcl-G has recently been implicated in oncogenesis in other tissues. The present study examines the hypothesis that reduced expression of these genes may be involved in prostate cancer. METHODS. Fau and Bcl-G mRNA levels were determined by real time RT-PCR in two independent prostate tissue collections. In experiments in vitro, Fau and Bcl-G levels in prostate cancer cell lines were reduced using RNA interference and the effects on sensitivity to UVC irradiation were determined. RESULTS. Fau and Bcl-G mRNA levels were both lower in prostate cancer tissue than in normal prostate and Benign Prostate Hyperplasia. Active down-regulation of Fau and Bcl-G expression in vitro resulted in decreased sensitivity to UVC-induced cytotoxicity. Simultaneous down-regulation of Fau and Bcl-G produced a decrease in sensitivity which was similar to either gene alone. CONCLUSIONS. Fau and Bcl-G mRNA levels are both decreased in prostate cancer. In prostate cancer cell lines in vitro such down-regulation results in reduced sensitivity to UVC-induced cytotoxicity, consistent with the putative roles of these genes as candidate prostate tumor suppressors. The absence of an additive effect when Fau and Bcl-G were down-regulated simultaneously is consistent with the two genes acting in the same apoptosis pathway, for example, with the pro-apoptotic effects of Fau being mediated through modulation of Bcl-G. Prostate 70: 1513-1523, 2010. (C) 2010 Wiley-Liss, Inc.en_US
dc.format.extent1513 - 1523en_US
dc.languageEnglishen_US
dc.language.isoEnglishen_US
dc.publisherWILEY-LISSen_US
dc.titleApoptosis Regulators Fau and Bcl-G Are Down-Regulated in Prostate Canceren_US
dc.typeJournal Article
rioxxterms.versionofrecord10.1002/pros.21186en_US
rioxxterms.licenseref.startdate2010-10-01en_US
rioxxterms.typeJournal Article/Reviewen_US
dc.relation.isPartOfPROSTATEen_US
pubs.notesaffiliation: Williams, GT (Reprint Author), Keele Univ, Inst Sci & Technol Med, Sch Life Sci, Huxley Bldg, Keele ST5 5BG, Staffs, England. Pickard, Mark R.; Williams, Gwyn T., Keele Univ, Inst Sci & Technol Med, Sch Life Sci, Keele ST5 5BG, Staffs, England. Edwards, Sandra E.; Cooper, Colin S., Inst Canc Res, Mol Carcinogenesis Sect, Sutton, Surrey, England. keywords: apoptosis; BCL2L14; Fau; oncogenesis; prognosis keywords-plus: EXPRESSION CLONING REVEALS; FUNCTIONAL EXPRESSION; ANDROGEN RECEPTOR; PROTEIN; GENE; RESISTANCE; FAMILY; CARCINOGENESIS; HYPERPLASIA; INVOLVEMENT research-areas: Endocrinology & Metabolism; Urology & Nephrology web-of-science-categories: Endocrinology & Metabolism; Urology & Nephrology author-email: g.t.williams@keele.ac.uk orcid-numbers: Williams, Gwyn/0000-0003-4556-9930 funding-acknowledgement: Biotechnology and Biological Sciences Research Council; National Cancer Research Institute Prostate Cancer Collaborative of the United Kingdom; Medical Research Council [G0802851] funding-text: We thank Professor NJ Maitland, University of York, UK for the gift of PNT2C2 and P4E6 cell lines, and the Biotechnology and Biological Sciences Research Council and the National Cancer Research Institute Prostate Cancer Collaborative of the United Kingdom for funding. number-of-cited-references: 36 times-cited: 8 usage-count-last-180-days: 0 usage-count-since-2013: 4 journal-iso: Prostate doc-delivery-number: 657IF unique-id: ISI:000282405700003 da: 2018-08-17en_US
pubs.notesNot knownen_US
pubs.organisational-group/ICR
pubs.organisational-group/ICR/Primary Group
pubs.organisational-group/ICR/Primary Group/ICR Divisions
pubs.organisational-group/ICR/Primary Group/ICR Divisions/Closed research teams
pubs.organisational-group/ICR/Primary Group/ICR Divisions/Closed research teams/Cell Transformation
pubs.volume70en_US
pubs.embargo.termsNot knownen_US
icr.researchteamCell Transformationen_US
dc.contributor.icrauthorCooper, Colinen_US
dc.contributor.icrauthorEdwards, Sandraen_US


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