ER Stress Negatively Modulates the Expression of the miR-199a214 Cluster to Regulates Tumor Survival and Progression in Human Hepatocellular Cancer 英文参考文献.docVIP

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ER Stress Negatively Modulates the Expression of the miR-199a214 Cluster to Regulates Tumor Survival and Progression in Human Hepatocellular Cancer 英文参考文献.doc

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ER Stress Negatively Modulates the Expression of the miR-199a214 Cluster to Regulates Tumor Survival and Progression in Human Hepatocellular Cancer 英文参考文献

ERStressNegativelyModulatestheExpressionofthe miR-199a/214ClustertoRegulatesTumorSurvivaland ProgressioninHumanHepatocellularCancer QuanluDuan1,XingxuWang1,WeiGong1,LiNi1,ChenChen1*,XingxingHe2,FuqiongChen1,LeiYang1, PeihuaWang1,DaoWenWang1* 1DepartmentofInternalMedicineandGeneTherapyCenter,HuazhongUniversityofScienceandTechnology,Wuhan,People’sRepublicofChina,2InstituteofLiver Diseases,TongjiHospital,TongjiMedicalCollege,HuazhongUniversityofScienceandTechnology,Wuhan,People’sRepublicofChina Abstract Background: Recent studies have emphasized causative links between microRNAs (miRNAs) deregulation and tumor development. In hepatocellular carcinoma (HCC), more and more miRNAs were identified as diagnostic and prognostic cancerbiomarkers,aswellasadditionaltherapeutictools.Thisstudyaimedtoinvestigatethefunctionalsignificanceand regulatorymechanismofthemiR-199a2/214clusterinHCCprogression. Methods and Findings: In this study, we showed that miR-214, as well as miR-199a-3p and miR-199a-5p levels were significantlyreducedinthemajorityofexamined23HCCtissuesandHepG2andSMMC-7721celllines,comparedwiththeir nontumorcounterparts.TofurtherexploretheroleofmiR-214inhepatocarcinogenesis,wedisclosedthattheERstress- induced pro-survival factor XBP-1 is a target of miR-214 by using western blot assay and luciferase reporter assay. Re- expression of miR-214 in HCC cell lines (HepG2 and SMMC-7721) inhibited proliferation and induced apoptosis. Furthermore,ectopicexpressionofmiR-214dramaticallysuppressedtheabilityofHCCcellstoformcoloniesinvitroandto developtumorsinasubcutaneousxenotransplantationmodeloftheBALB/cathymicnudemice.Moreover,reintroduction of XBP-1s attenuated miR-214-mediated suppression of HCC cells proliferation, colony and tumor formation. To further understand the mechanism of the miR-199a/214 cluster down-expression in HCC, we found that thapsigargin (TG) and tunicamycin (TM) or hypoxia-induced unfolded protein response (UPR) suppresses the expression of the miR-199a/