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1、MedOncol(2016)33:21DOI10.1007/s12032-016-0734-zORIGINALPAPEREpigeneticregulationofE-cadherinexpressionbythehistonedemethylaseUTXincoloncancercells1,22221LinZha•QiangCao•XinCui•FenfenLi•HoujieLiang•22BingzhongXue•HangShiReceived:9November2015/Accepted:11J
2、anuary2016ÓSpringerScience+BusinessMediaNewYork2016AbstractDecreasedepithelialcadherin(E-cadherin)decreasedH3K27me3attheE-cadherinpromoter.Further,geneexpression,ahallmarkofepithelialmesenchymalUTXinteractedwiththehistoneacetyltransferase(HAT)transition(
3、EMT),isessentialfortriggeringmetastaticproteinCBPandrecruitedittotheE-cadherinpromoter,advantageofthecoloncancer.GeneticmechanismsresultinginincreasedH3K27acetylation(H3K27ac),aunderlyingtheregulationofE-cadherinexpressioninEMThistonetranscriptionalactiv
4、emark.UTXpositivelyregu-havebeenextensivelyinvestigated;however,muchislatesE-cadherinexpressionthroughcoordinatedregulationunknownabouttheepigeneticmechanismunderlyingthisofH3K27demethylationandacetylation,switchingtheprocess.Here,weidentifiedubiquitously
5、transcribedtranscriptionalrepressivestatetothetranscriptionalactivetetratricopeptiderepeatonchromosomeX(UTX),ahis-stateattheE-cadherinpromoter.WeconcludethatUTXtonedemethylaseinvolvedindemethylatingdi-ortri-mayplayaroleinregulationofE-cadheringeneexpress
6、ionmethylatedhistone3lysine27(H3K27me2/3),asaposi-inHCT-116cellsandthatUTXmayserveasatherapeutictiveregulatorfortheexpressionofE-cadherininthecolontargetagainstthemetastasisinthetreatmentofcoloncancercelllineHCT-116.Weshowedthatinactivationofcancer.UTXdo
7、wn-regulatedE-cadheringeneexpression,whileoverexpressionofUTXdidtheopposite.Notably,over-KeywordsHistonedemethylaseH3K27UTXEMTexpressionofUTXinhibitedmigrationandinvasionofE-cadherinColoncancerHCT-116cells.Moreover,UTXdemethylatedH3K27me3,ahistonetr
8、anscriptionalrepressivemark,leadingtoIntroductionColoncancerisamajorcauseofcancermortalityandisElectronicsupplementarymaterialTheonlineversionofthisoneofthemostcommoncancersintheUSA[1,2].Colonarticle(doi:10.1007/s12032-016
