In addition, MiR-200c has been shown to suppress EMT, to attribute to the targeting of ZEB1/ZEB2, repressors of the cell-cell contact protein E-cadherin, and to mainly regulate the cellular epithelial and interstitial state conversion to finish the typical phenotype changes of EMT in the process of tumor cell growth [10, 17, 18]. This evidence concerns the gene CDH1 and neoplasm.