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Diminished expression of phosphatidylethanolamine N-methyltransferase 2 during hepatocarcinogenesis.

ABSTRACT: Phosphatidylethanolamine N-methyltransferase (PEMT) is a liver-specific enzyme that converts phosphatidylethanolamine into phosphatidylcholine. At least two forms of PEMT are present in hepatocytes. However, PEMT activity is negligible in two hepatoma cell lines. Previous studies have indicated an inverse relationship between the expression of one form, PEMT2, and the rate of liver growth, suggesting that this enzyme might be involved in inhibition of hepatocyte proliferation. We have now investigated the expression of PEMT2 at various stages of hepatocarcinogenesis induced by chemical carcinogens. Expression of PEMT2 protein was decreased in liver samples that contained the first detectable proliferative lesions. At later stages of carcinogenesis, PEMT2 expression was obliterated. PEMT activity decreased, the levels of PEMT2 mRNA decreased and there was an increase in the activity of CTP:phosphocholine cytidylyltransferase, a key regulatory enzyme in the CDP-choline pathway of phosphatidylcholine biosynthesis. Southern blot analyses of restriction fragments of DNA showed no changes in the PEMT gene in hepatocarcinoma compared with normal liver. A role for PEMT2 in the control of hepatocyte proliferation remains an intriguing possibility.

SUBMITTER: Tessitore L

PROVIDER: S-EPMC1219931 | biostudies-other | 1999 Jan

REPOSITORIES: biostudies-other

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Project description:AIM:Through exploring the regulation of gene expression during hepatocarcinogenesis induced by aflatoxin B(1) (AFB(1)), to find out the responsible genes for hepatocellular carcinoma (HCC) and to further understand the underlying molecular mechanism. METHODS:Tree shrews (Tupaia belangeri chinensis) were treated with or without AFB(1) for about 90 weeks. Liver biopsies were performed regularly during the animal experiment. Eight shares of total RNA were respectively isolated from 2 HCC tissues, 2 HCC-surrounding non-cancerous liver tissues, 2 biopsied tissues at the early stage (30th week) of the experiment from the same animals as above, 1 mixed sample of three liver tissues biopsied at the beginning (0th week) of the experiment, and another 1 mixed sample of two liver tissues from the untreated control animals biopsied at the 90th week of the experiment. The samples were then tested with the method of Atlas(TM) cDNA microarray assay. The levels of gene expression in these tissues taken at different time points during hepatocarcinogenesis were compared. RESULTS:The profiles of differently expressed genes were quite different in different ways of comparison. At the same period of hepatocarcinogenesis, the genes in the same function group usually had the same tendency for up- or down-regulation. Among the checked 588 genes that were known to be related to human cancer, 89 genes (15.1%) were recognized as "important genes" because they showed frequent changes in different ways of comparison. The differentially expressed genes during hepatocarcinogenesis could be classified into four categories: genes up-regulated in HCC tissue, genes with similar expressing levels in both HCC and HCC-surrounding liver tissues which were higher than that in the tissues prior to the development of HCC, genes down-regulated in HCC tissue, and genes up-regulated prior to the development of HCC but down-regulated after the development of HCC. CONCLUSION:A considerable number of genes could change their expressing levels both in HCC and in HCC-surrounding non-cancerous liver tissues. A few modular genes were up-regulated only in HCC but not in surrounding liver tissues, while some apoptosis-related genes were down-regulated in HCC and up-regulated in surrounding liver tissues. To compare gene-expressing levels among the liver tissues taken at different time points during hepatocarcinogenesis may be helpful to locate the responsible gene (s) and understand the mechanism for AFB(1) induced liver cancer.

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Diminished expression of phosphatidylethanolamine N-methyltransferase 2 during hepatocarcinogenesis.

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