CDK5RAP3 Is a Novel Repressor of p14ARF in Hepatocellular Carcinoma Cells 英文参考文献.docVIP

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CDK5RAP3 Is a Novel Repressor of p14ARF in Hepatocellular Carcinoma Cells 英文参考文献.doc

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CDK5RAP3 Is a Novel Repressor of p14ARF in Hepatocellular Carcinoma Cells 英文参考文献

CDK5RAP3IsaNovelRepressorofp14ARF in HepatocellularCarcinomaCells GraceWing-YanMak1,Wai-LungLai1.,YuanZhou1.,MingtaoLi4,IreneOi-LinNg2,3,Yick-PangChing1,3 * 1DepartmentofAnatomy,LiKaShingFacultyofMedicine,TheUniversityofHongKong,HongKong,China,2DepartmentofPathology,LiKaShingFacultyofMedicine, The University of Hong Kong, Hong Kong, China, 3State Key Laboratory for Liver Research, The University of Hong Kong, Hong Kong, China, 4Department of PharmacologyandtheProteomicsCenter,ZhongshanSchoolofMedicine,SunYat-senUniversity,Guangzhou,Guangdong,China Abstract CDK5 regulatory subunit associated protein 3 (CDK5RAP3) is a novel activator of PAK4 and processes important pro- metastatic function in hepatocarcinogenesis. However, it remains unclear if there are other mechanisms by which CDK5RAP3promotesHCCmetastasis.Here,weshowedthatinCDK5RAP3stableknockdownSMMC-7721HCCcells,p14ARF tumorsuppressorwasupregulatedatproteinandmRNAlevels,andectopicexpressionofCDK5RAP3wasfoundtorepress thetranscriptionofp14ARF.Usingchromatinimmunoprecipitationassay,wedemonstratedthatCDK5RAP3boundtop14ARF promoterinvivo.Furthermore,knockdownofp14ARFinCDK5RAP3stableknockdownHCCcellsreversedthesuppressionof HCCcellinvasivenessmediatedbyknockdownofCDK5RAP3.Takentogether,ourfindingsprovidethenewevidencethat overexpressionofCDK5RAP3promotesHCCmetastasisviadownregulationofp14ARF . Citation:MakGW-Y,LaiW-L,ZhouY,LiM,NgIO-L,etal.(2012)CDK5RAP3IsaNovelRepressorof p14ARF inHepatocellularCarcinomaCells.PLoSONE7(7): e42210.doi:10.1371/journal.pone.0042210 Editor:Xin-yuanGuan,TheUniversityofHongKong,China ReceivedJanuary18,2012;AcceptedJuly5,2012;PublishedJuly31,2012 Copyright:?2012Maketal.Thisisanopen-accessarticledistributedunderthetermsoftheCreativeCommonsAttributionLicense,whichpermitsunrestricted use,distribution,andreproductioninanymedium,providedtheoriginalauthorandsourcearecredited. Funding:OurresearchisfinanciallysupportedbyTheHongKongResearchGrantCouncil(N_HKU715/08and7/CRF/09)(webpage:.