Genome-Wide Expression of MicroRNAs Is Regulated by DNA Methylation in Hepatocarcinogenesis

Figure 2

UCSC genome browser tracks showing histone modification (H3K4me1, H3K4me3, and H3K27ac) and DNase I cleavage states around the hypermethylated CpG sites of mir-125b-1 and mir-199a-1 in the HepG2 cell line and in seven other cancer cell lines. The genome browser map from top to bottom is the CpG island; layered H3K4Me1 and H3K4Me3 marks in the seven other cancer cell lines; H3K4Me3, H3K4Me1, and H3K27Ac marks and DNase I hypersensitive sites in HepG2 cells; H3K27Ac activator in seven cancer cell lines; and GC percent. (a) Genomic region around mir-125b-1 (chr11:121,962,000-121,976,000). Consistent with DNA hypermethylation and underexpression of miR-125b, no active histone marks (H3K4me1, H3K4me3, and H3K27ac) and DNase I hypersensitive sites were observed in HepG2 cells, but higher levels of H3K4me1, H3K4me3, and H3K27ac were found at the same region in the seven other cancer cell lines. (b) The genomic region around mir-199a-1 (chr19:10,917,000-10,933,000). Consistent with DNA hypermethylation and underexpression of miR-199a, there was no activation of histone markers (H3K4me1, H3K4me3, and H3K27ac), as well as closed chromatin (no peak for DNase I hypersensitive sites) in HepG2 cells, which is different from the pattern observed in the other cancer cell lines (showing high to intermediate peaks for H3K4me1, H3K4me3, and H3K27ac marks).

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