538《癌症》ChineseJournalofCancer，2006，25（5）：538-542·基础研究·17β-雌二醇调控子宫内膜癌细胞孤儿核受体ERRα表达的研究高敏，孙蓬明，赵丹，王建六，李小平，魏丽惠RegulatoryEffectof17β-EstradiolonExpressionofOrphanNuclearReceptorERRαinEndometrialCarcinomaCellLinesGAOMin，SUNPeng-Ming，ZHAODan，WANGJian-Liu，LIXiao-Ping，WEILi-Hui［ABSTRACT］BACKGROUND&OBJECTIVE：Estrogenreceptor-relatedreceptorα（ERRα），amemberofthesubfamilyoforphannuclearreceptors，couldcompetewithestrogenreceptorα（ERα）tobindthesametargetgenesandinterfereinERsignalpathway.Therefore，itmightbeassociatedtothetumorigenesisofendometrialcarcinoma.Thisstudywastoexploretheregulatoryeffectof17β-estradiol（17β-E2）onERRαexpression，andtoelucidatetherelationshipbetweenERRαandERsignalpathwayinendometrialcarcinomacelllines.METHODS：ERα-positivecelllineIshikawaandERα-negativecelllineHEC-IAweretreatedwithdifferentconcentrations-10-8-6of17β-E2（1×10mol/L，1×10mol/L，and1×10mol/L）for24hand48h，respectively.ThelevelsofERRαmRNAandproteinwereexaminedbyreversetranscription-polymerasechainreaction（RT-PCR）andWesternblot.-8-617β-E2（1×10mol/L）andcompleteERinhibitorICI182，780（1×10mol/北京大学人民医院L）weregivenconcomitantlytoobservethechangeofERRαexpression.妇科RESULTS：ThelevelsofERRαmRNAandproteininIshikawacellswere北京100044down-regulatedafterstimulatedfor24hand48hbydifferentconcentrations-8of17β-E2.Themaximaleffectwasobservedattheconcentrationof1×10DepartmentofGynecology，mol/L.When17β-E2andICI182，780weregivensimultaneouslytoIshikawacells，thisdown-regulationwasblocked.However，thelevelofERRαmRNA，People1sHospital，PekingUniversity，notprotein，inHEC-IAcellswasup-regulatedafterstimulatedbydifferentBeijing，100044，concentrationsof17β-E2for24h.Afterstimulatedby17β-E2for48h，theP.R.ChinalevelofERRαproteinwasup-regulated，whichcouldnotbeblockedbyICI182，780.CONCLUSIONS：17β-E2candown-regulatetheexpressionof通讯作者：魏丽惠ERRαinIshikawacells，whichismediatedbyERα.17β-E2canup-regulateCorrespondenceto：WEILi-HuitheexpressionofERRαinHEC-IAcells，butthisregulationcannotbeTel：86-10-68792701block