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. 2020 Oct 14;42(7):1171–1179. doi: 10.1038/s41401-020-00543-x

Fig. 5. Overexpression of EZH2 inhibited the expression of FOXC1 by increasing H3K27me3 level.

Fig. 5

a Overexpression of EZH2 resulted in the methylation of histone H3 and the formation of H3K27me3, which inhibited the expression of FOXC1. b The knockdown of EZH2 expression reduced the levels of H3K27me3 and increased the expression of FOXC1 in MCF-7 cells. c The knockdown of EZH2 expression reduced the expression of H3K27me3 and increased the expression of FOXC1 in T47D cells. d Neither H3K27me3 nor FOXC1 expression was changed in HCC1806 EZH1 cells overexpressing EZH1 compared to control cells. e Neither H3K27me3 nor FOXC1 expression was changed in HCC1806 EZH1 shRNA cells, in which EZH1 was downregulated compared to control cells. The experiments were performed in triplicate. f In silico analysis from ENCODE showed that the H3K27me3 antibody can bind to the promoter region of the FOXC1 gene. g ChIP with H3K27me3 antibodies or control IgG showed that H3K27me3 antibodies bound to the promoter of the FOXC1 gene.