Carcinogenesis, Vol. 20, No. 4, 561-567,
April 1999
© 1999 Oxford University Press
Expression of phosphatidylethanolamine N-methyltransferase in Yoshida ascites hepatoma cells and the livers of host rats
Dipartimento di Scienze Cliniche e Biologiche, Università degli Studi di Torino, Torino, Italy and
1 Lipid and Lipoprotein Research Group and Department of Biochemistry, University of Alberta, Edmonton, Alberta T6G 2S2, Canada
2 Present address: Dipartimento di Scienze Mediche, Università del Piemonte Orientale `Amedeo Avogadro', Viale Ferrucci 33, 28100 Novara, Italy
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.
Abbreviations: 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.
3 To whom correspondence should be addressed at: Dipartimento di Scienze Cliniche e Biologiche, Ospedale S.Luigi Gonzaga, Regione Gonzole 10, 10043 Orbassano (TO), Italy Email: tessitor{at}pasteur.sluigi.unito.it
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