title: MiR-200a inhibits epithelial-mesenchymal transition of pancreatic cancer stem cell.
abstract: BACKGROUND
  Pancreatic cancer is one of the most aggressive cancers, and the aggressiveness of pancreatic cancer is in part due to its intrinsic and extrinsic drug resistance characteristics, which are also associated with the acquisition of epithelial-to-mesenchymal transition (EMT). Increasing evidence suggests that EMT-type cells share many biological characteristics with cancer stem-like cells. And miR-200 has been identified as a powerful regulator of EMT.
  
  
  METHODS
  Cancer Stem Cells (CSCs) of human pancreatic cancer cell line PANC-1 were processed for CD24, CD44 and ESA multi-colorstaining, and sorted out on a BD FACS Aria II machine. RT-qPCR was performed using the miScript PCR Kit to assay the expression of miR-200 family. In order to find the role of miR-200a in the process of EMT, miR-200a mimic was transfected to CSCs.
  
  
  RESULTS
  Pancreatic cancer cells with EMT phenotype displayed stem-like cell features characterized by the expression of cell surface markers CD24, CD44 and epithelial-specific antigen (ESA), which was associated with decreased expression of miR-200a. Moreover, overexpression of miR-200a was resulted in down-regulation of N-cadherin, ZEB1 and vimentin, but up-regulation of E-cadherin. In addition, miR-200a overexpression inhibited cell migration and invasion in CSCs.
  
  
  CONCLUSIONS
  In our study, we found that miR-200a played an important role in linking the characteristics of cancer stem-like cells with EMT-like cell signatures in pancreatic cancer. Selective elimination of cancer stem-like cells by reversing the EMT phenotype to mesenchymal-to-epithelial transition (MET) phenotype using novel agents would be useful for prevention and/or treatment of pancreatic cancer.
authors: Yuhua
authors: Y
authors: Lu
authors: Jingjing
authors: J
authors: Lu
authors: Xiaohong
authors: X
authors: Li
authors: Hui
authors: H
authors: Zhu
authors: Xiangjun
authors: X
authors: Fan
authors: Shajun
authors: S
authors: Zhu
authors: Yao
authors: Y
authors: Wang
authors: Qingsong
authors: Q
authors: Guo
authors: Lei
authors: L
authors: Wang
authors: Yan
authors: Y
authors: Huang
authors: Department of General Surgery, Affiliated Hospital of Nantong University, Nantong, Jiangsu Province 226001, P, R, China. zmy5661@163.com.
authors: Mingyan
authors: M
authors: Zhu
authors: Zhiwei
authors: Z
authors: Wang
mesh_terms: D045744:Cell Line, Tumor; D002465:Cell Movement / Q000502:physiology; D058750:Epithelial-Mesenchymal Transition / Q000502:physiology*; D005434:Flow Cytometry / Q000379:methods; D006801:Humans; D035683:MicroRNAs / Q000096:biosynthesis*; D014411:Neoplastic Stem Cells / Q000378:metabolism* / Q000473:pathology; D010190:Pancreatic Neoplasms / Q000378:metabolism* / Q000473:pathology
chemical_list: C533896:MIRN200 microRNA, human; D035683:MicroRNAs