Disturbance of DNA methylation patterns in the early phase of hepatocarcinogenesis induced by a choline-deficient L-amino acid-defined diet in rats

Cancer Sci. 2007 Sep;98(9):1318-22. doi: 10.1111/j.1349-7006.2007.00564.x. Epub 2007 Jul 19.

Abstract

The authors investigated the DNA methylation patterns of the E-cadherin, Connexin 26 (Cx26), Rassf1a and c-fos genes in the early phase of rat hepatocarcinogenesis induced by a choline-deficient L-amino acid-defined (CDAA) diet. Six-week-old F344 male rats were continuously fed with the CDAA diet, and three animals were then killed at each of 4 and 8 days and 3 weeks. Genomic DNA was extracted from livers for assessment of methylation status in the 5' upstream regions of E-cadherin, Cx26, Rassf1a and c-fos genes by bisulfite sequencing, compared with normal livers. The livers of rats fed the CDAA diet for 4 and 8 days and 3 weeks were methylated in E-cadherin, Cx26 and Rassf1a genes, while normal livers were all unmethylated. In contrast, normal livers were highly methylated in c-fos gene. Although the livers at 4 days were weakly methylated, those at 8 days and 3 weeks were markedly unmethylated. Methylation patterns of CpG sites in E-cadherin, Cx26 and Rassf1a were sparse and the methylation was not associated with gene repression. These results indicate that gene-specific DNA methylation patterns were found in livers of rats after short-term feeding of the CDAA diet, suggesting gene-specific hypermethylation might be involved in the early phase of rat hepatocarcinogenesis induced by the CDAA diet.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Amino Acids / administration & dosage
  • Amino Acids / metabolism*
  • Animals
  • Cadherins / genetics
  • Cadherins / metabolism
  • Carcinoma, Hepatocellular / etiology
  • Carcinoma, Hepatocellular / genetics*
  • Carcinoma, Hepatocellular / metabolism*
  • Choline Deficiency / complications
  • Choline Deficiency / genetics
  • Choline Deficiency / metabolism*
  • Connexin 26
  • Connexins / genetics
  • Connexins / metabolism
  • DNA (Cytosine-5-)-Methyltransferase 1
  • DNA (Cytosine-5-)-Methyltransferases / biosynthesis
  • DNA (Cytosine-5-)-Methyltransferases / genetics
  • DNA Methylation*
  • Diet / adverse effects*
  • Gene Expression Regulation, Neoplastic
  • Liver Neoplasms, Experimental / etiology
  • Liver Neoplasms, Experimental / genetics*
  • Liver Neoplasms, Experimental / metabolism*
  • Male
  • Proto-Oncogene Proteins c-fos / genetics
  • Proto-Oncogene Proteins c-fos / metabolism
  • Rats
  • Rats, Inbred F344
  • Tumor Suppressor Proteins / genetics
  • Tumor Suppressor Proteins / metabolism

Substances

  • Amino Acids
  • Cadherins
  • Connexins
  • Gjb2 protein, rat
  • Proto-Oncogene Proteins c-fos
  • Tumor Suppressor Proteins
  • Connexin 26
  • DNA (Cytosine-5-)-Methyltransferase 1
  • DNA (Cytosine-5-)-Methyltransferases