Antagonism of miR-21 Reverses Epithelial-Mesenchymal Transition and Cancer Stem Cell Phenotype through AKTERK12 Inactivation by Targeting PTEN 英文参考文献.docVIP

下载本文档

3
0
约4.34万字
约 11页
2017-05-11 发布于上海
举报
版权申诉

Antagonism of miR-21 Reverses Epithelial-Mesenchymal Transition and Cancer Stem Cell Phenotype through AKTERK12 Inactivation by Targeting PTEN 英文参考文献.doc

1、本文档共11页，可阅读全部内容。
2、原创力文档（book118）网站文档一经付费（服务费），不意味着购买了该文档的版权，仅供个人/单位学习、研究之用，不得用于商业用途，未经授权，严禁复制、发行、汇编、翻译或者网络传播等，侵权必究。
3、本站所有内容均由合作方或网友上传，本站不对文档的完整性、权威性及其观点立场正确性做任何保证或承诺！文档内容仅供研究参考，付费前请自行鉴别。如您付费，意味着您自己接受本站规则且自行承担风险，本站不退款、不进行额外附加服务；查看《如何避免下载的几个坑》。如果您已付费下载过本站文档，您可以点击这里二次下载。
4、如文档侵犯商业秘密、侵犯著作权、侵犯人身权等，请点击“版权申诉”（推荐），也可以打举报电话：400-050-0827(电话支持时间：9:00-18:30)。
5、该文档为VIP文档，如果想要下载，成为VIP会员后，下载免费。
6、成为VIP后，下载本文档将扣除1次下载权益。下载后，不支持退款、换文档。如有疑问请联系我们。
7、成为VIP后，您将拥有八大权益，权益包括：VIP文档下载权益、阅读免打扰、文档格式转换、高级专利检索、专属身份标志、高级客服、多端互通、版权登记。
8、VIP文档为合作方或网友上传，每下载1次，网站将根据用户上传文档的质量评分、类型等，对文档贡献者给予高额补贴、流量扶持。如果你也想贡献VIP文档。上传文档

Antagonism of miR-21 Reverses Epithelial-Mesenchymal Transition and Cancer Stem Cell Phenotype through AKTERK12 Inactivation by Targeting PTEN 英文参考文献

AntagonismofmiR-21ReversesEpithelial-Mesenchymal TransitionandCancerStemCellPhenotypethrough AKT/ERK1/2InactivationbyTargetingPTEN MingliHan1,2,ManranLiu2,YimengWang3,XinChen1,JianliXu4,YanSun2,LiuyangZhao2,HongboQu1, YuanmingFan1,ChengyiWu1* 1Department of Endocrine Surgery, The First Affiliated Hospital of Chongqing Medical University, Chongqing, China, 2The Key Laboratory of Laboratory Medical DiagnosticsintheMinistryofEducationandDepartmentofClinicalBiochemistry,ChongqingMedicalUniversity,Chongqing,China,3DepartmentofEmergency,TheFirst AffiliatedHospitalofChongqingMedicalUniversity,Chongqing,China,4DepartmentofGeneralSurgery,ThePeople’sHospitalofJiangjinCity,Chongqing,China Abstract Background: Accumulating evidencesuggested that epithelial-mesenchymal transition (EMT)and cancer stemcell (CSC) characteristics,bothofwhichcontributetotumorinvasionandmetastasis,areinterrelatedwithmiR-21.MiR-21isoneofthe importantmicroRNAsassociatedwithtumorprogressionandmetastasis,butthemolecularmechanismsunderlyingEMT andCSCphenotypeduringmiR-21contributestomigrationandinvasionofbreastcancercellsremaintobeelucidated. Methodology/PrincipalFindings:Inthisstudy,MDA-MB-231/anti-miR-21cellswereestablishedbytransfectedhsa-miR-21 antagomir into breast cancer MDA-MB-231 cells. EMT was evaluated by the changes of mesenchymal cell markers (N- cadherin,Vimentin,andalpha-SMA),epithelialcellmarker(E-cadherin),aswellascapacitiesofcellmigrationandinvasion; CSC phenotype was measured using the changes of CSC surface markers (ALDH1 and CD44), and the capacity of sphereforming (mammospheres). We foundthat antagonism of miR-21 reversed EMT andCSC phenotype, accompanied with PTEN up-regulation and AKT/ERK1/2 inactivation. Interestingly, down-regulation of PTEN by siPTEN suppressed the effectsofmiR-21antagomironEMTandCSCphenotype,confirmingthatPTENisatargetofmiR-21inreversingEMTand CSCphenotype.TheinhibitorsofPI3K-AKTandERK1/2pathways,LY294002andU0126,bothsignificantlysuppressedEMT andCSCphenotype,i