FOXA1 Promotes Tumor Progression in Prostate Cancer via the Insulin-Like Growth Factor Binding Protein 3 Pathway 英文参考文献.docVIP

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FOXA1 Promotes Tumor Progression in Prostate Cancer via the Insulin-Like Growth Factor Binding Protein 3 Pathway 英文参考文献.doc

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FOXA1 Promotes Tumor Progression in Prostate Cancer via the Insulin-Like Growth Factor Binding Protein 3 Pathway 英文参考文献

FOXA1PromotesTumorProgressioninProstateCancer viatheInsulin-LikeGrowthFactorBindingProtein3 Pathway YusukeImamura1,ShinichiSakamoto1*,TakumiEndo2,TakanobuUtsumi1,MikiFuse1, TakahitoSuyama1,KojiKawamura1,TakashiImamoto1,KojiroYano3,KatsuhiroUzawa4,NaokiNihei1, HiroyoshiSuzuki2,AtsushiMizokami5,TakeshiUeda6,NaohikoSeki7,HidekiTanzawa4, TomohikoIchikawa1 1DepartmentofUrology,ChibaUniversityGraduateSchoolofMedicine,Chiba,Japan,2DepartmentofUrology,TohoUniversityMedicalCenterSakuraHospital,Chiba, Japan, 3Faculty of Information Science and Technology, Osaka Institute of Technology, Osaka, Japan, 4Department of Clinical Molecular Biology, Chiba University GraduateSchoolofMedicine,Chiba,Japan,5DepartmentofUrology,KanazawaUniversityGraduateSchoolofMedicalSciences,Ishikawa,Japan,6ProstateCenterand DivisionofUrology,ChibaCancerCenter,Chiba,Japan,7DepartmentofFunctionalGenomics,ChibaUniversityGraduateSchoolofMedicine,Chiba,Japan Abstract Fork-headboxproteinA1(FOXA1)isa‘‘pioneerfactor’’thatisknowntobindtotheandrogenreceptor(AR)andregulate thetranscriptionofAR-specificgenes.However,thepreciseroleofFOXA1inprostatecancer(PC)remainsunknown.Inthis study,wereportthatFOXA1playsacriticalroleinPCcellproliferation.TheexpressionofFOXA1washigherinPCthanin normalprostatetissues(P=0.0002),and,usingimmunohistochemicalanalysis,wefoundthatFOXA1waslocalizedinthe nucleus.FOXA1expressionlevelsweresignificantlycorrelatedwithbothPSAandGleasonscores(P=0.016andP=0.031, respectively). Moreover, FOXA1 up-regulation was a significant factor in PSA failure (P=0.011). Depletion of FOXA1 in aprostatecancercellline(LNCaP)usingsmallinterferingRNA(siRNA)significantlyinhibitedARactivity,ledtocell-growth suppression, and induced G0/G1 arrest. The anti-proliferative effect of FOXA1 siRNA was mediated through insulin-like growth factor binding protein 3 (IGFBP-3). An increase in IGFBP-3, mediated by depletion of FOXA1, inhibited phosphorylationofMAPKandAkt,andincreasedexpressionofthecellcycleregulatorsp21andp27.