SIRNA-Directed In Vivo Silencing of Androgen Receptor Inhibits the Growth of Castration-Resistant Prostate Carcinomas 英文参考文献.docVIP

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SIRNA-Directed In Vivo Silencing of Androgen Receptor Inhibits the Growth of Castration-Resistant Prostate Carcinomas 英文参考文献.doc

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SIRNA-Directed In Vivo Silencing of Androgen Receptor Inhibits the Growth of Castration-Resistant Prostate Carcinomas 英文参考文献

SIRNA-DirectedInVivoSilencingofAndrogenReceptor InhibitstheGrowthofCastration-ResistantProstate Carcinomas DanielCompagno1.,CaroleMerle1.,Aure′lieMorin1.,Criste`leGilbert1,JacquesR.R.Mathieu1,AlineBozec2,ClaireMauduit2 ,Mohammed Benahmed2,FlorenceCabon1* 1CNRS,UniversityParis-Sud,FRE2944,EpigeneticsandCancer,InstitutAndre′ Lwoff,Villejuif,France,2INSERMU406,Lyon,France Background.Prostatecarcinomasareinitiallydependentonandrogens,andcastrationorandrogenantagonistsinhibittheir growth.Aftersometimethough,tumorsbecomeresistantandrecurwithapoorprognosis.Themajorityofresistanttumors stillexpressesafunctionalandrogenreceptor(AR),frequentlyamplifiedormutated. Methodology/Principal Findings.To test the hypothesis that ARisnot only expressed, but isstill a keytherapeutic target in advanced carcinomas, weinjected siRNAtargetingARintomicebearingexponentiallygrowingcastration-resistanttumors.QuantificationofsiRNAintotumors andmousetissuesdemonstratedtheirefficientuptake.ThisuptakesilencedARintheprostate,testesandtumors.ARsilencing intumorsstronglyinhibitedtheirgrowth,andimportantly,alsomarkedlyrepressedtheVEGFproductionandangiogenesis. Conclusions/Significance.Ourresultsdemonstratethatcarcinomasresistanttohormonalmanipulationsstilldependonthe expressionoftheandrogenreceptorfortheirdevelopmentinvivo.ThesiRNA-directedsilencingofAR,whichallowstargeting overexpressedaswellasmutatedisoforms,triggersastrongantitumoralandantiangiogeniceffect.siRNA-directedsilencingof thiskeygeneinadvancedandresistantprostatetumorsopenspromisingnewtherapeuticperspectivesandtools. Citation: CompagnoD,MerleC,MorinA,GilbertC,MathieuJRR,etal(2007)SIRNA-Directed InVivoSilencingofAndrogenReceptorInhibitsthe GrowthofCastration-ResistantProstateCarcinomas.PLoSONE2(10):e1006.doi:10.1371/journal.pone.0001006 INTRODUCTION become truly androgen-independent [11]. Thus, although AR is functional in most recurrent tumors [5,12], disrupting AR signaling once theresistant phenotypeisestablished, may