antagonism of mir-21 reverses epithelial-mesenchymal transition and cancer stem cell phenotype through akterk12 inactivation by targeting ptenmir-21拮抗逆转epithelial-mesenchymal过渡和癌症干细胞表型通过akterk12针对pten的失活.pdfVIP

Antagonism of miR-21 Reverses Epithelial-Mesenchymal Transition and Cancer Stem Cell Phenotype through AKT/ERK1/2 Inactivation by Targeting PTEN 1,2 2 3 1 4 2 2 1 Mingli Han , Manran Liu , Yimeng Wang , Xin Chen , Jianli Xu , Yan Sun , Liuyang Zhao , Hongbo Qu , 1 1 Yuanming Fan , Chengyi Wu * 1 Department of Endocrine Surgery, The First Affiliated Hospital of Chongqing Medical University, Chongqing, China, 2 The Key Laboratory of Laboratory Medical Diagnostics in the Ministry of Education and Department of Clinical Biochemistry, Chongqing Medical University, Chongqing, China, 3 Department of Emergency, The First Affiliated Hospital of Chongqing Medical University, Chongqing, China, 4 Department of General Surgery, The People’s Hospital of Jiangjin City, Chongqing, China Abstract Background: Accumulating evidence suggested that epithelial-mesenchymal transition (EMT) and cancer stem cell (CSC) characteristics, both of which contribute to tumor invasion and metastasis, are interrelated with miR-21. MiR-21 is one of the important microRNAs associated with tumor progression and metastasis, but the molecular mechanisms underlying EMT and CSC phenotype during miR-21 contributes to migration and invasion of breast cancer cells remain to be elucidated. Methodology/Principal Findings: In this study, MDA-MB-231/anti-miR-21 cells were established by transfected hsa-miR-21 antagomir into breast cancer MDA-MB-231 cells. EMT was evaluated by the changes of mesenchymal cell markers (N- cadherin, Vimentin, and alpha-SMA), epithelial cell marker (E-cadherin), as well as capacities of cell migration and invasion; CSC phenotype was measured using the changes of CSC