Methionine metabolism and cancer.
This paper summarizes recent developments linking methionine metabolism and S-adenosylmethionine to DNA methylation and gene expression in relation to cancer. Methionine, obtained in the diet and synthesized by several reactions in the body, is the sole precursor of S-adenosylmethionine, the primary methyl donor in the body. Disruptions in methionine metabolism and methylation reactions may be involved in cancer processes. S-Adenosylmethionine is involved in, inter alia, the methylation of a small percentage of cytosine bases of DNA. Recent evidence suggests that enzymatic DNA methylation is an important component of gene control and may serve as a silencing mechanism for gene function. Some carcinogens interfere with enzymatic DNA methylation, and thus may allow oncogene activation. Demethylation may be a necessary, but not always sufficient, condition for enhanced transcription. DNA hypomethylation has been observed in many cancer cells and tumors. The hypothesis that oncogenic transformation may be prevented or even reversed by a diet containing excess methionine and/or choline needs to be further investigated.
D000818:Animals; D050940:Betaine-Homocysteine S-Methyltransferase; D004032:Diet; D005786:Gene Expression Regulation; D008322:Mammals; D008715:Methionine / Q000378:metabolism*; D008745:Methylation; D008780:Methyltransferases / Q000378:metabolism; D008954:Models, Biological; D009369:Neoplasms / Q000378:metabolism*; D012436:S-Adenosylmethionine / Q000378:metabolism
D012436:S-Adenosylmethionine; D008715:Methionine; D008780:Methyltransferases; D050940:Betaine-Homocysteine S-Methyltransferase