Nuclear Factor-κB–Dependent Epithelial to Mesenchymal Transition Induced by HIF-1α Activation in Pancreatic Cancer Cells under Hypoxic Conditions 英文参考文献.docVIP

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Nuclear Factor-κB–Dependent Epithelial to Mesenchymal Transition Induced by HIF-1α Activation in Pancreatic Cancer Cells under Hypoxic Conditions 英文参考文献.doc

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Nuclear Factor-κB–Dependent Epithelial to Mesenchymal Transition Induced by HIF-1α Activation in Pancreatic Cancer Cells under Hypoxic Conditions 英文参考文献

NuclearFactor-kB–DependentEpithelialtoMesenchymal TransitionInducedbyHIF-1aActivationinPancreatic CancerCellsunderHypoxicConditions Zhuo-XinCheng1,BeiSun1*,Shuang-JiaWang1,YueGao2,Ying-MeiZhang3,Hao-XinZhou1,GuangJia1, Yong-WeiWang1,RuiKong1,Shang-HaPan1,Dong-BoXue1,Hong-ChiJiang1,Xue-WeiBai1 1DepartmentofPancreaticandBiliarySurgery,TheFirstAffiliatedHospitalofHarbinMedicalUniversity,Harbin,People’sRepublicofChina,2DepartmentofSurgery, University Hospitals, Case Western Reserve University, Cleveland, Ohio, United States of America, 3Central Laboratory, The First Affiliated Hospital of Harbin Medical University,Harbin,People’sRepublicofChina Abstract Background:Epithelialtomesenchymaltransition(EMT)inducedbyhypoxiaisoneofthecriticalcausesoftreatmentfailure in different types of human cancers. NF-kB is closely involved in the progression of EMT. Compared with HIF-1a , the correlationbetweenNF-kBandEMTduringhypoxiahasbeenlessstudied,andalthoughthephenomenonwasobservedin thepast,themolecularmechanismsinvolvedremainedunclear. Methodology/PrincipalFindings:Here,wereportthathypoxiaoroverexpressionofhypoxia-induciblefactor-1a(HIF-1a) promotes EMT in pancreatic cancer cells. On molecular or pharmacologic inhibition of NF-kB, hypoxic cells regained expressionofE-cadherin,lostexpressionofN-cadherin,andattenuatedtheirhighlyinvasiveanddrug-resistantphenotype. Introducing a pcDNA3.0/HIF-1a into pancreatic cancer cells under normoxic conditions heightened NF-kB activity, phenocopying EMT effects produced by hypoxia. Conversely, inhibiting the heightened NF-kB activity in this setting attenuatedtheEMTphenotype. Conclusions/Significance:TheseresultssuggestthathypoxiaoroverexpressionofHIF-1ainducestheEMTthatislargely dependentonNF-kBinpancreaticcancercells. Citation:ChengZ-X,SunB,WangS-J,GaoY,ZhangY-M,etal.(2011)NuclearFactor-kB–DependentEpithelialtoMesenchymalTransitionInducedbyHIF-1a ActivationinPancreaticCancerCellsunderHypoxicConditions.PLoSONE6(8):e23752.doi:10.1371/journal.po