Journal Article

Expression of phosphatidylethanolamine <i>N</i>-methyltransferase in Yoshida ascites hepatoma cells and the livers of host rats

Luciana Tessitore, Eliana Sesca, Martino Bosco and Dennis E. Vance

in Carcinogenesis

Volume 20, issue 4, pages 561-567
Published in print April 1999 | ISSN: 0143-3334
Published online April 1999 | e-ISSN: 1460-2180 | DOI: http://dx.doi.org/10.1093/carcin/20.4.561
Expression of phosphatidylethanolamine N-methyltransferase in Yoshida ascites hepatoma cells and the livers of host rats

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Previous studies have implicated phosphatidylethanolamine N-methyltransferase-2 (PEMT2) in the regulation of non-neoplastic liver growth [Tessitore,L., Cui,Z. and Vance,E. (1997) Biochem. J., 322, 151–154]. We have now investigated whether or not PEMT2 is also involved in the control of proliferation of hepatoma cells growing in an animal and cell death by apoptosis in the liver of tumor-bearing rats. PEMT activity was barely detectable and PEMT2 protein was absent in hepatoma cells growing exponentially in vivo whereas CTP:phosphocholine cytidylyltransferase (CT) activity and expression were high. The lack of PEMT2 corresponded with the absence of its mRNA. Both PEMT2 protein and mRNA appeared when cells entered the stationary phase of tumor growth and, in parallel, CT expression decreased. The host liver first became hyperplastic and exhibited a slight increase in CT activity and decrease in PEMT2 expression. During the stationary phase of hepatoma growth the host liver regressed and eventually became hypoplastic following induction of apoptosis. The appearance of apoptosis in the host liver was associated with a marked reduction in both CT activity and expression as well as an enhancement of PEMT activity and PEMT2 expression. McArdle RH7777 hepatoma cells underwent apoptosis when transfected with cDNA for PEMT2. The evidence supports the proposal that PEMT2 may have a role in the regulation of `in vivo' hepatoma and hepatocyte cell division as well as hepatocyte cell death by apoptosis.

Keywords: ALT, alanine aminotransferase; CDP, cytidine diphosphate; CHO, Chinese hamster ovary; CT, CTP:phosphocholine cytidylyltransferase; DMEM, Dulbecco's modified Eagle's medium; GAPDH, glyceraldehyde 3-phosphate dehydrogenase; PBS, phosphate-buffered saline; PC, phosphatidylcholine; PEMT, phosphatidylethanolamine N-methyltransferase; PKC, protein kinase C; TUNEL, TdT-mediated dUTP nick end labeling.

Journal Article.  5671 words.  Illustrated.

Subjects: Clinical Cytogenetics and Molecular Genetics

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