MiR-200a Inhibits Epithelial-Mesenchymal Transition of Pancreatic Cancer Stem Cell

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  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 epithelialto-mesenchymal transition.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.In this study, we found that 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,which was associated with decreased expression of miR-200a.Moreover,overexpression of miR-200a was resulted in down-regulation of N-cadherin, ZEB 1 and vimentin, but up-regulation of E-cadherin.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 phenotype using novel agents would be useful for prevention and/or treatment of pancreatic cancer.
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