Fig. 8
From: Expression signatures and roles of microRNAs in inflammatory breast cancer
Schema of miR-205 regulated ZEB1, ZEB2, EMT pathway. A model for the regulatory mechanism of EMT by Mel-18. Loss of Mel-18 in breast cancer leads to hypermethylation of the CGrich region of the miR-205 promoter by regulating recruitment of DNMT family proteins to the miR-205 proximal promoter, and results in downregulation of miR-205 expression. This epigenetic repression of miR-205 leads to upregulation of the target genes, ZEB1 and ZEB2, and consequently activates ZEB1- and ZEB2-mediated repression of E-cadherin transcription. Thus, loss of E-cadherin by the miR-205/ZEB1-ZEB2 cascade following Mel-18 depletion in breast cancer induces the EMT and tumor invasion