title: MiR-206 suppresses epithelial mesenchymal transition by targeting TGF-β signaling in estrogen receptor positive breast cancer cells.
abstract: BACKGROUND
  Previous reports have shown a mutual negative feedback loop between microRNA (miR)-206 and estrogen receptor (ER) expression. Furthermore, decreased miR-206 expression in breast cancer (BC) is associated with the advanced clinical stage and lymph node metastasis. However, its role and the mechanism underlying the migration and invasion of ER positive BC remain unclear.
  
  
  RESULTS
  In this study, miR-206 was stably transfected into ER positive cell lines MCF-7 and T47D to investigate the effect of miR-206. The results showed that miR-206 overexpression markedly impaired the migration and invasive abilities of these cells, followed by suppression of the epithelial mesenchymal transition (EMT). Mechanistic analyses showed that miR-206 inhibited the autocrine production of transforming growth factor (TGF)-β as well as the downstream expression of neuropilin-1 (NRP1) and SMAD2, responsible for the decreased migration, invasion, and EMT in these cells.
  
  
  CONCLUSIONS
  Our data demonstrate that miR-206 inhibits TGF-β transcription and autocrine production, as well as downstream target genes of EMT. Restoring miR-206 expression may provide an effective therapeutic strategy for ER positive BC.
authors.affiliation: Department of Breast Surgery, Fudan University Shanghai Cancer Center, Shanghai, China.|Department of Oncology, Shanghai Medical College, Fudan University, Shanghai, China.
authors.forename: Kai
authors.initials: K
authors.lastname: Yin
authors.affiliation: Department of Breast Surgery, Fudan University Shanghai Cancer Center, Shanghai, China.|Department of Oncology, Shanghai Medical College, Fudan University, Shanghai, China.
authors.forename: Wenjin
authors.initials: W
authors.lastname: Yin
authors.affiliation: Department of Oncology, Shanghai Medical College, Fudan University, Shanghai, China.
authors.forename: Yaohui
authors.initials: Y
authors.lastname: Wang
authors.affiliation: Department of Oncology, Shanghai Medical College, Fudan University, Shanghai, China.
authors.forename: Liheng
authors.initials: L
authors.lastname: Zhou
authors.affiliation: Department of Oncology, Shanghai Medical College, Fudan University, Shanghai, China.
authors.forename: Yu
authors.initials: Y
authors.lastname: Liu
authors.affiliation: Breast Cancer Center, Renji Hospital, School of Medicine, Shanghai Jiaotong University, Shanghai, China.|Central Laboratory, The Fifth People's Hospital of Shanghai, Fudan University, Shanghai, China.
authors.forename: Gong
authors.initials: G
authors.lastname: Yang
authors.affiliation: Breast Cancer Center, Renji Hospital, School of Medicine, Shanghai Jiaotong University, Shanghai, China.
authors.forename: Jianhua
authors.initials: J
authors.lastname: Wang
authors.affiliation: Department of Oncology, Shanghai Medical College, Fudan University, Shanghai, China.
authors.forename: Jinsong
authors.initials: J
authors.lastname: Lu
mesh_terms: D020413:3' Untranslated Regions / Q000235:genetics; D001943:Breast Neoplasms / Q000235:genetics / Q000378:metabolism / Q000473:pathology; D045744:Cell Line, Tumor; D002465:Cell Movement / Q000187:drug effects / Q000235:genetics; D058750:Epithelial-Mesenchymal Transition / Q000235:genetics*; D020869:Gene Expression Profiling / Q000379:methods; D015972:Gene Expression Regulation, Neoplastic / Q000187:drug effects*; D006801:Humans; D061986:MCF-7 Cells; D035683:MicroRNAs / Q000235:genetics*; D039942:Neuropilin-1 / Q000235:genetics / Q000378:metabolism; D011960:Receptors, Estrogen / Q000378:metabolism; D015398:Signal Transduction / Q000235:genetics*; D051899:Smad2 Protein / Q000235:genetics / Q000378:metabolism; D016212:Transforming Growth Factor beta / Q000494:pharmacology*
chemical_list: D020413:3' Untranslated Regions; C546087:MIRN206 microRNA, human; D035683:MicroRNAs; D011960:Receptors, Estrogen; D051899:Smad2 Protein; D016212:Transforming Growth Factor beta; D039942:Neuropilin-1
keywords: TGF-β; breast cancer; epithelial mesenchymal transition; miRNA; migration