IP of 5-methylcytosine (5-mc) enriched DNA fragments from control and mice with non-acoholic steatohepatitis (NASH) related hepatocellular carcinoma (HCC)

ABSTRACT: Through the analysis of mouse liver tumours promoted by distinct routes (DEN exposure alone, DEN exposure plus non-genotoxic insult with phenobarbital and non-alcoholic fatty liver disease); we report that the cancer associated hyper-methylated CGI events in mice are also predicated by silent promoters that are enriched for both the DNA modification 5-hydroxymethylcytosine (5hmC) and the histone modification H3K27me3 in normal liver. During cancer progression these CGIs undergo hypo-hydroxymethylation, prior to subsequent hyper-methylation; whilst retaining H3K27me3. A similar loss of promoter-core 5hmC is observed in Tet1 deficient mouse livers indicating that reduced Tet1 binding at CGIs may be responsible for the epigenetic dysregulation observed during hepatocarcinogenesis. Consistent

ORGANISM(S): Mus musculus

SUBMITTER: John Thomson 

PROVIDER: E-GEOD-77725 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress