title: miR-205 promotes epithelial-mesenchymal transition by targeting AKT signaling in endometrial cancer cells.
abstract: OBJECTIVE
  AKT signaling regulates multiple biological processes and expresses in various cancers. miR-205 plays complex roles in tumorigenesis and tumor progression by acting either as a tumor suppressor or an oncogene depending on the tumor type. Here we describe the molecular mechanism of miR-205 regulating epithelial-mesenchymal transition by activation of AKT signaling in endometrial cancer cells HEC-50B and HEC-1-A.
  
  
  METHODS
  The proliferation of HEC-50B cells transfected with miR-205 mimic was assessed by WST-1 assay. The migration and invasion were evaluated by BD transwell migration and matrigel invasion assays. The EMT markers were detected by Western blot.
  
  
  RESULTS
  We found that miR-205 increased the proliferation in HEC-50B cells. The migration and invasion of HEC-50B cells and HEC-1-A cells were enhanced by miR-205. When HEC-50B cells and HEC-1-A cells were treated with anti-miR-205 inhibitor, the migration and invasion were decreased as compared with the negative control. The overexpression of miR-205 inhibited E-cadherin expression and promoted Snail expression by activation of AKT and downregulation of glycogen synthase kinase 3β. However, after the HEC-50B cells and HEC-1-A cells were treated with anti-miR-205 inhibitor, E-cadherin expression was increased and Snail protein level was decreased by inhibition of AKT expression.
  
  
  CONCLUSIONS
  Our data strongly suggest that miR-205 plays an important role in endometrial cancer migration and invasion by targeting the AKT pathway. Our data highlight miR-205 as a potential molecular target for endometrial cancer treatment.
authors.affiliation: School of Medicine International Healthcare Center, Second Affiliated Hospital Zhejiang University, HangZhou, China.
authors.forename: Chenyu
authors.initials: C
authors.lastname: Jin
authors.affiliation: Department of Gynaecology, Zhejiang Provincial Hospital of Traditional Chinese Medicine, HangZhou, China.
authors.forename: Ruojia
authors.initials: R
authors.lastname: Liang
mesh_terms: D000230:Adenocarcinoma / Q000378:metabolism*; D045744:Cell Line, Tumor; D049109:Cell Proliferation; D016889:Endometrial Neoplasms / Q000378:metabolism*; D058750:Epithelial-Mesenchymal Transition; D005260:Female; D006801:Humans; D035683:MicroRNAs / Q000378:metabolism*; D009362:Neoplasm Metastasis; D051057:Proto-Oncogene Proteins c-akt / Q000378:metabolism*
chemical_list: D035683:MicroRNAs; D051057:Proto-Oncogene Proteins c-akt; C534425:MIR205, human
keywords: AKT; endometrial cancer; epithelial-mesenchymal transition; glycogen synthase kinase 3β; miR-205