title: Re-expression of miR-21 contributes to migration and invasion by inducing epithelial-mesenchymal transition consistent with cancer stem cell characteristics in MCF-7 cells.
abstract: MiR-21 is known to play an important role in the development and progression, including migration and invasion, of many malignancies including breast cancer. Accumulating evidence suggest that the induction of epithelial-mesenchymal transition (EMT) phenotype and acquisition of cancer stem cell (CSC) characteristics are highly interrelated, and contribute to tumorigenesis, tumor progression, metastasis, and relapse. The molecular mechanisms underlying EMT and CSC characteristics during miR-21 contributes to cell migration and invasion of breast cancer are poorly understood. Therefore, we established miR-21 re-expressing breast cancer MCF-7 (MCF-7/miR-21) cells, which showed increasing cell growth, migration and invasion, self-renewal and clonogenicity. Our data showed that re-expression of miR-21 induced the acquisition of EMT phenotype by activation of mesenchymal cell markers (N-cadherin, Vimentin, α-SMA) and inhibition of epithelial cell marker (E-cadherin) in MCF-7/miR-21 cells, which consistent with increased cell subpopulation expressing CSC surface markers (ALDH1(+) and CD44(+)/CD24(-/low)) and the capacity of sphereforming (mammospheres). Our results demonstrated that re-expression of miR-21 is responsible for migration and invasion by activating the EMT process and enhancing the characteristics of CSCs in MCF-7 cells.
authors.affiliation: Department of Endocrine Surgery, The First Affiliated Hospital of Chongqing Medical University, Chongqing 400016, China.
authors.forename: Mingli
authors.initials: M
authors.lastname: Han
authors.forename: Manran
authors.initials: M
authors.lastname: Liu
authors.forename: Yimeng
authors.initials: Y
authors.lastname: Wang
authors.forename: Zhiqiang
authors.initials: Z
authors.lastname: Mo
authors.forename: Xiaokai
authors.initials: X
authors.lastname: Bi
authors.forename: Zhirong
authors.initials: Z
authors.lastname: Liu
authors.forename: Yuanming
authors.initials: Y
authors.lastname: Fan
authors.forename: Xin
authors.initials: X
authors.lastname: Chen
authors.forename: Chengyi
authors.initials: C
authors.lastname: Wu
mesh_terms: D000199:Actins / Q000378:metabolism; D000080924:Aldehyde Dehydrogenase 1 Family; D015703:Antigens, CD / Q000378:metabolism; D014408:Biomarkers, Tumor / Q000378:metabolism; D001943:Breast Neoplasms / Q000235:genetics* / Q000378:metabolism / Q000473:pathology*; D051927:CD24 Antigen / Q000378:metabolism; D015820:Cadherins / Q000378:metabolism; D045744:Cell Line, Tumor; D002465:Cell Movement / Q000235:genetics*; D049109:Cell Proliferation; D058750:Epithelial-Mesenchymal Transition / Q000235:genetics*; D005260:Female; D015972:Gene Expression Regulation, Neoplastic; D006801:Humans; D018960:Hyaluronan Receptors / Q000378:metabolism; D007527:Isoenzymes / Q000378:metabolism; D035683:MicroRNAs / Q000378:metabolism*; D009361:Neoplasm Invasiveness; D014411:Neoplastic Stem Cells / Q000378:metabolism* / Q000473:pathology*; D051059:PTEN Phosphohydrolase / Q000378:metabolism; D010641:Phenotype; D050697:Retinal Dehydrogenase / Q000378:metabolism; D018874:Spheroids, Cellular; D013997:Time Factors; D014162:Transfection; D014746:Vimentin / Q000378:metabolism
chemical_list: C541116:ACTA2 protein, human; D000199:Actins; D015703:Antigens, CD; D014408:Biomarkers, Tumor; D051927:CD24 Antigen; C497889:CD24 protein, human; C497483:CD44 protein, human; C513384:CDH1 protein, human; C050361:CDH2 protein, human; D015820:Cadherins; D018960:Hyaluronan Receptors; D007527:Isoenzymes; C524940:MIRN21 microRNA, human; D035683:MicroRNAs; D014746:Vimentin; D000080924:Aldehyde Dehydrogenase 1 Family; C510223:ALDH1A1 protein, human; D050697:Retinal Dehydrogenase; D051059:PTEN Phosphohydrolase; C494929:PTEN protein, human