Silencing Prion Protein in MDA-MB-435 Breast Cancer Cells Leads to Pleiotropic Cellular Responses to Cytotoxic Stimuli 英文参考文献.docVIP

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Silencing Prion Protein in MDA-MB-435 Breast Cancer Cells Leads to Pleiotropic Cellular Responses to Cytotoxic Stimuli 英文参考文献.doc

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Silencing Prion Protein in MDA-MB-435 Breast Cancer Cells Leads to Pleiotropic Cellular Responses to Cytotoxic Stimuli 英文参考文献

SilencingPrionProteininMDA-MB-435BreastCancer CellsLeadstoPleiotropicCellularResponsestoCytotoxic Stimuli GuohuaYu1*.,LimingJiang1*.,YuanyuanXu1.,HongweiGuo1,HuiyanLiu1,YiZhang1,2,HuaiyiYang3, ChonggangYuan1,JiyanMa1,2* 1SchoolofLifeSciences,KeyLaboratoryofBrainFunctionalGenomics,MinistryofEducation,ShanghaiKeyLaboratoryofBrainFunctionalGenomics,EastChinaNormal University,Shanghai,China,2DepartmentofMolecularandCellularBiochemistry,OhioStateUniversity,Columbus,Ohio,UnitedStatesofAmerica,3CASKeyLaboratory ofPathogenicMicrobiologyandImmunology,InstituteofMicrobiology,ChineseAcademyofSciences,Beijing,China Abstract Prionprotein(PrP)iswellstudiedforitspathogenicroleinpriondisease,butitspotentialcontributiontootherpathological processes is less understood. PrP is expressed in a variety of cancers and at least in pancreatic and breast cancers, its expressionappearstobeassociatedwithpoorprognosis.TounderstandtheroleofPrPinbreastcancercells,weknocked downPrPexpressioninMDA-MB-435breastcancercellswithsmallinterferingRNAandsubjectedthesecellstoaseriesof analyses.WefoundthatPrPknockdowninthesecellsdoesnotaffectcellproliferationorcolonyformation,butsignificantly influencesthecellularresponsetocytotoxicstimuli.Comparedtocontrolcells,PrPknockdowncellsexhibitedanincreased susceptibilitytoserumdeprivationinducedapoptosis,nochangetostaurosporine-orpaclitaxel-inducedcelldeaths,anda reducedsusceptibilitytochemotherapydrugdoxorubicin-inducedcelldeath.Tounderstandthemechanismofunexpected roleofPrPinexacerbatingdoxorubicin-inducedcytotoxicity,weanalyzedcelldeathrelatedBcl-2familyproteins.Wefound that PrP knockdown alters the expression of several Bcl-2 family proteins, correlating with increased resistance to doxorubicin-inducedcytotoxicity.Moreover,theenhanceddoxorubicinresistanceisindependentofDNAdamagerelated p53pathway,butatleastpartiallythroughtheERK1/2pathway.Together,ourstudyrevealedthatsilencingPrPinMDA-MB- 435 breast cancer cells results in very different responses to various