CancerLetters364(2015)33–43
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CancerLetters
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OriginalArticles
MiR-429increasesthemetastaticcapabilityofHCCviaregulating
classicWntpathwayratherthanepithelial–mesenchymaltransition
JingTanga,b,1,LiangLia,b,1,WentaoHuanga,c,1,ChengjunSuib,YingchengYanga,
XimengLina,GuojunHoua,XinChena,JingFua,ShengxianYuanb,ShaoLid,WenWena,
ShanhuaTanga,DanCaoa,MengchaoWua,b,LeiChena,b,*,HongyangWanga,b,e,**
aNationalCenterforLiverCancer,Shanghai,
bEasternHepatobiliarySurgeryHospital,SecondMilitaryMedicalUniversity,Shanghai200438,
cGraduateSchoolofFujianMedicalUniversity,Fuzhou,FujianProvince350108,
dBioinformaticsDivision,TNLIST/DepartmentofAutomation,TsinghuaUniversity,Beijing100084,
eNationalLaboratoryforOncogenesandRelatedGenes,CancerInstitute,RuijinHospital,ShanghaiJiaoTongUniversity,Shanghai200441,
ARTICLEINFO
Articlehistory:EpigeneticmodificationofmiR-429canmanipulateliverT-ICsviatargetingtheRBBP4/E2F1/Oct4axis,
Received18February2015whichmightbecrucialforhepatocarcinogenesis.However,whethermiR-429playsaroleinregulating
Receivedinrevisedform18April2015metastasisofhepatocellularcarcinomaisstillunclear.Usingquantitativemethylationanalysisandreal-
Accepted20April2015
timePCR,wehaveidentifiedthehypomethylatedstatusandupregulationofmiR-429inportalvein
metastasissam
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