E-Cadherin Is Transcriptionally Activated via Suppression of ZEB1 Transcriptional Repressor by Small RNA-Mediated Gene Silencing 英文参考文献.docVIP

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E-Cadherin Is Transcriptionally Activated via Suppression of ZEB1 Transcriptional Repressor by Small RNA-Mediated Gene Silencing 英文参考文献.doc

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E-Cadherin Is Transcriptionally Activated via Suppression of ZEB1 Transcriptional Repressor by Small RNA-Mediated Gene Silencing 英文参考文献

E-CadherinIsTranscriptionallyActivatedviaSuppression ofZEB1TranscriptionalRepressorbySmallRNA- MediatedGeneSilencing MinamiMazda,KenjiNishi,YukiNaito,KumikoUi-Tei* DepartmentofBiophysicsandBiochemistry,GraduateSchoolofScience,UniversityofTokyo,Tokyo,Japan Abstract RNAactivationhasbeenreportedtobeinducedbysmallinterferingRNAs(siRNAs)thatactonthepromotersofseveral genescontainingE-cadherin.Inthisstudy,wepresentanalternativemechanismofE-cadherinactivationinhumanPC-3 cellsbysiRNAspreviouslyreportedtopossessperfect-complementarysequencestoE-cadherinpromoter.Wefoundthat activationofE-cadherincanbealsoinducedviasuppressionofZEB1,whichisatranscriptionalrepressorofE-cadherin,by seed-dependentsilencingmechanismofthesesiRNAs.Thefunctionalseed-complementarysitesofthesiRNAswerefound inthecodingregioninadditiontothe39untranslatedregionofZEB1mRNA.PromoteranalysesindicatedthatE-boxes, whichareZEB1-bindingsites,intheupstreampromoterregionareindispensableforE-cadherintranscriptionbythesiRNAs. Thus, the results caution against ignoring siRNA seed-dependent silencing effects in genome-wide transcriptional regulation. In addition, members of miR-302/372/373/520 family, which have the same seed sequences with one of the siRNAs containing perfect-complementarity to E-cadherin promoter, are also found to activate E-cadherin transcription. Thus,E-cadherincouldbeupregulatedbythesuppressionofZEB1transcriptionalrepressorbymiRNAsinvivo. Citation:MazdaM,NishiK,NaitoY,Ui-TeiK(2011)E-CadherinIsTranscriptionallyActivatedviaSuppressionofZEB1TranscriptionalRepressorbySmallRNA- MediatedGeneSilencing.PLoSONE6(12):e28688.doi:10.1371/journal.pone.0028688 Editor:AkioKanai,KeioUniversity,Japan ReceivedOctober14,2011;AcceptedNovember13,2011;PublishedDecember21,2011 Copyright: ? 2011 Mazda et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricteduse,distribution,andreproductioninanymedium,providedtheoriginalauthorandsourcearecr