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Am J Physiol Gastrointest Liver Physiol 280: G184-G190, 2001;
0193-1857/01 $5.00
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Vol. 280, Issue 2, G184-G190, February 2001

Role of promoter methylation in increased methionine adenosyltransferase 2A expression in human liver cancer

Heping Yang1, Zong-Zhi Huang1, Zhaohui Zeng1, Changjin Chen1, Robert R. Selby2, and Shelly C. Lu1

1 Division of Gastroenterology and Liver Diseases, USC Liver Disease Research Center, and 2 Hepatobiliary/Pancreas and Liver Transplant Surgery, Department of Surgery, University of Southern California School of Medicine, Los Angeles, California 90033

Methionine adenosyltransferase (MAT), an essential enzyme that catalyzes the formation of S-adenosylmethionine (SAM), is encoded by two genes, MAT1A (liver-specific) and MAT2A (non-liver-specific). We showed a switch from MAT1A to MAT2A expression in human liver cancer, which facilitates cancer cell growth. The present work examined the role of methylation in MAT2A transcriptional regulation. We found that the human MAT2A promoter is hypomethylated in hepatocellular carcinoma, in which the gene is upregulated transcriptionally, but hypermethylated in normal liver, in which the gene is minimally expressed. Luciferase activities driven by in vitro methylated MAT2A promoter constructs were 75-95% lower than activities driven by unmethylated constructs. SAM treatment of Hep G2 cells reduced MAT2A endogenous expression by 75%, hypermethylated the MAT2A promoter, and reduced luciferase activities driven by MAT2A promoter constructs by 65-75% while not affecting MAT1A's promoter activity. Treatment of adult rat and human hepatocytes with trichostatin A, an inhibitor of histone deacetylase, upregulated MAT2A expression by more than fourfold. Collectively, these results suggest that MAT2A expression is regulated by promoter methylation and histone acetylation.

methionine adenosyltransferase 1A; S-adenosylmethionine; transcriptional regulation; transient transfection


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