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. 2017 Jul 10;6(7):e356. doi: 10.1038/oncsis.2017.59

Figure 6.

Figure 6

Epigenetic silencing of miR-137 by MeCP2 and DNMTs reactivated ASCT2 expression. (a) Binding of MeCP2 and DNMTs to the miR-137 CpG island analyzed by ChIP assay in HCT116 cells. The ACTIN promoter was used as a negative control. Results were presented as averages of fold changes between MeCP2, DNMT1, DNMT3B ChIP and isotype IgG controls. P1, primer set 1; P2, primer set 2; P3, primer set 3. Mean±s.d. (n=3), t-test; *P<0.05. (b–e) Effects of MeCP2 depletion or 5′-Aza-CdR treatment on miR-137 (b, d) and ASCT2 expression (c, e) in HCT116 and T98G cells. Actin was used as a loading control. Mean±s.d. (n=3), t-test; **P<0.01. (f, g) Binding of MeCP2 and DNMT3B to the miR-137 CpG island analyzed by ChIP assay in HCT116 cells upon MeCP2 depletion (f) or 5′-Aza-CdR treatment (g). Results were presented as averages of fold changes between MeCP2, DNMT3B ChIP and isotype IgG controls. Mean±s.d. (n=3), t-test; *P<0.05, **P<0.01.