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1、Wangetal.JournalofExperimental&ClinicalCancerResearch(2016)35:100DOI10.1186/s13046-016-0379-yRESEARCHOpenAccessTRIM11overexpressionpromotesproliferation,migrationandinvasionoflungcancercellsXiaolinWang,WeipingShi,HongcanShi,ShichunLu,KangWang,ChaoSun,JianshengHe,WeiguoJin,XiaoxiaLv,
2、*HuiZouandYushengShuAbstractBackground:TripartiteMotifContaining11(TRIM11),amemberofTRIMproteins,isoverexpressedinhigh-gradegliomasandplaysanoncogenicfunctioningliomabiology.However,littleisknownabouttheroleofTRIM11inlungcancer.Methods:WeanalyzedTRIM11mRNAexpressioninlungcancertissu
3、esandadjacentnon-neoplastictissuesbyreal-timePCR.WethenexploredthefunctionofTRIM11inlungcancercellsbysmallinterferingRNA-mediateddownregulationofthisproteinfollowedbyanalysesofcellproliferation,migrationandinvasion.Results:TRIM11washighlyexpressedinlungcancertissuesandlungcancercell
4、lines.ThehigherexpressionofTRIM11wascorrelatedwiththepoorerprognosisofpatients.SuppressingofTRIM11expressioninlungcancercellswithhigherexpressionofTRIM11(A549andNCI-H446cells)significantlyreducedcellgrowth,motilityandinvasiveness.WefurtherdemonstratedthatknockdownofTRIM11affectedthe
5、expressionofcellproliferation-relatedproteins(CyclinD1andPCNA),andepithelial-mesenchymaltransformation-relatedproteins(VEGF,MMP-2,MMP-9,Twist1,SnailandE-cadherin).TheactivityofERKandPI3K/AKTwasalsosuppressedinTRIM11knockeddowncells.FurtherexperimentsinlungcellswithlowerexpressionofT
6、RIM11(NCI-H460andNCI-H1975cells)withAKTinhibitorsuggestedthatTRIM11maypromotecellmotilityandinvasivenessthroughAKTpathway.Conclusions:OurresultsindicatethatTRIM11actsasanoncogeneinlungcancerthroughpromotingcellgrowth,migrationandinvasion.Ourfindingsmayhaveimportantimplicationforthed
7、etectionandtreatmentoflungcancer.Keywords:TRIM11,Lungcancer,PI3K/AKT,Migration,InvasionBackgroundproteinsareactiveinlungtumorprogressionwillcontrib-Lungcanceristhemostfrequentlydiagnosedmalignancy.utetothedevelopmentofearlydetectionandtargetedItistheleadingcauseofcancerdeathwithover
8、1milliontherapyforl
