Fig. 6: Promoters of a set of genes were hyper-methylated in ADI1-overexpressing cells. | Cell Death & Disease

Fig. 6: Promoters of a set of genes were hyper-methylated in ADI1-overexpressing cells.

From: The methionine salvage pathway-involving ADI1 inhibits hepatoma growth by epigenetically altering genes expression via elevating S-adenosylmethionine

Fig. 6

a Heat map representation of DNA methylation levels in J7 cell with or without ADI1 overexpression. b The genomic features of hyper-methylated sites in ADI1-overexpressing cells. c The distributions of significant hypermethylation in total promoters (upper), promoters for protein coding genes (upper middle), promoters for non-coding RNA genes (lower middle), and promoters for miRNA genes (lower). Horizontal axis, chromosome numbers; vertical axis, p value. d The proposed growth regulatory mechanism obtained from this study. In non-cancerous hepatocytes, ADI (gray oval) levels were high, promoting MTA cycle to generate a large amount of SAMe, which in term modulated genome-wide promoter methylation to achieve a gene expression pattern for tumor suppression. In cancerous hepatocytes, ADI1 was reduced, leading to reduction of SAMe concentrations and thus alterations of genome methylation pattern. As a result, several oncogenes (such as CAV1), lncRNA, and miRNA were activated to promote cancer cell growth

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