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. 2011 Aug 29;31(16):2062–2074. doi: 10.1038/onc.2011.383

Figure 3.

Figure 3

Dynamic epigenetic regulation of miR-200 expression during in vitro induced EMT and MET. (a) The epithelial MDCK cells underwent morphological changes toward a mesenchymal phenotype (EMT) during TGFβ treatment that was reverted after TGFβ withdrawal (mesenchymal to epithelial transition, MET). (b) Progressive gain of CpG methylation in both clusters of miR-200 family during TGFβ-induced EMT, revealed by bisulfite genomic sequencing. The original unmethylated status was re-established in cells undergoing MET after TGFβ withdrawal. In all, 20 single clones were evaluated in each experimental condition. Presence of unmethylated or methylated CpGs is indicated by white or black squares, respectively. (c) Decreased expression of mature miR-200 family members during TGFβ treatment (Student's t-test P<0.05), which was recovered after TGFβ withdrawal, analyzed by qRT–PCR. (d) Restored expression of miR-200 in TGFβ-treated cells is achieved upon treatment with DNA-demethylating agent 5-aza-2′-deoxycytidine (aza), evaluated by qRT–PCR of mature miR-200 family members (Student's t-test P<0.05).