CHIP Regulates AKTFoxOBim Signaling in MCF7 and MCF10A Cells.docVIP

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CHIP Regulates AKTFoxOBim Signaling in MCF7 and MCF10A Cells.doc

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CHIP Regulates AKTFoxOBim Signaling in MCF7 and MCF10A Cells

CHIPRegulatesAKT/FoxO/BimSignalinginMCF7and MCF10ACells YanrongLv1,ShanshanSong2,KaiZhang1,HaidongGao1*,RongMa1* 1DepartmentofBreastSurgery,QiLuHospitalofShandongUniversity,Jinan,Shandong,China,2DepartmentofMolecularMicrobiologyandImmunology,Universityof SouthernCalifornia,LosAngeles,California,UnitedStatesofAmerica Abstract A number of studies have shown that apoptosis resistance can be observed in multiple human tumors; however the detailedmechanism remainsunclear.Inthepresentstudy,wedemonstratedthattheabnormaloverexpressionoftheC terminus of Hsc70-interacting protein (CHIP) induced apoptosis resistance by regulating the AKT/FoxO/Bim signaling pathwayinthebreastcancercellMCF7andthehumannon-tumorigeniccellMCF10A.WefoundthatCHIPoverexpression inMCF7andMCF10AcellsactivatedAKTandinhibitedtheForkheadboxO(FoxO)transcriptionfactorsFoxO1,FoxO3,and FoxO4,therebyinhibitingtranscriptionofthetargetgenesbimandpten.InhibitionofPI3Kbyachemicalreagentrevealed thattheseeventsmaybecriticalforCHIP-inducedapoptosisresistance.WealsodeterminedthatinhibitionofFoxO3by CHIPledtothedecreaseinPTENandfurtheractivatedtheAKTsurvivalpathway.Wecorroboratedourfindingsinbreast cancertissues.Ingeneral,theCHIP-modulatedAKT/FoxO/Bimsignalingpathwaywasshowntoinduceapoptosisresistance bydecreasingtheproteinlevelofthetumorsuppressorPTENinbothtranscriptionalandpost-translationalregulations. Citation:LvY,SongS,ZhangK,GaoH,MaR(2013)CHIPRegulatesAKT/FoxO/BimSignalinginMCF7andMCF10ACells.PLoSONE8(12):e83312.doi:10.1371/ journal.pone.0083312 Editor:JunLi,SunYat-senUniversityMedicalSchool,China ReceivedJune30,2013;AcceptedNovember1,2013;PublishedDecember23,2013 Copyright:?2013Lvetal.Thisisanopen-accessarticledistributedunderthetermsoftheCreativeCommonsAttributionLicense,whichpermitsunrestricted use,distribution,andreproductioninanymedium,providedtheoriginalauthorandsourcearecredited. Funding:ThesourceoffundingthathassupportedthisworkistheNatureScienceofShandongProvince,Q2008C08(/portal/).The fundershadnorole