Shimizu Kyoko, Onishi Mariko, Sugata Eriko, Sokuza Yui, Mori Chiharu, Nishikawa Tomoki, Honoki Kanya, Tsujiuchi Toshifumi
Laboratory of Cancer Biology and Bioinformatics, Department of Life Science, Faculty of Science and Engineering, Kinki University, 3-4-1 Kowakae, Higashiosaka, Osaka 577-8502, Japan.
Cancer Sci. 2007 Sep;98(9):1318-22. doi: 10.1111/j.1349-7006.2007.00564.x. Epub 2007 Jul 19.
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.
作者研究了胆碱缺乏的L-氨基酸限定(CDAA)饮食诱导的大鼠肝癌发生早期阶段E-钙黏蛋白、连接蛋白26(Cx26)、Rassf1a和c-fos基因的DNA甲基化模式。六周龄的F344雄性大鼠持续喂食CDAA饮食,然后在第4天、第8天和第3周分别处死三只动物。从肝脏中提取基因组DNA,通过亚硫酸氢盐测序评估E-钙黏蛋白、Cx26、Rassf1a和c-fos基因5'上游区域的甲基化状态,并与正常肝脏进行比较。喂食CDAA饮食4天、8天和3周的大鼠肝脏中,E-钙黏蛋白、Cx26和Rassf1a基因发生甲基化,而正常肝脏均未甲基化。相反,正常肝脏中c-fos基因高度甲基化。虽然第4天的肝脏甲基化程度较弱,但第8天和第3周的肝脏甲基化程度明显降低。E-钙黏蛋白、Cx26和Rassf1a中CpG位点的甲基化模式稀疏,且甲基化与基因抑制无关。这些结果表明,短期喂食CDAA饮食的大鼠肝脏中发现了基因特异性的DNA甲基化模式,提示基因特异性高甲基化可能参与了CDAA饮食诱导的大鼠肝癌发生早期阶段。