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Laboratory/Clinical Translational Research

Expression of Phosphatidylethanolamine N-Methyltransferase in Human Hepatocellular Carcinomas

Tessitore L.a · Marengo B.b · Vance D.E.c · Papotti M.d · Mussa A.d · Daidone M.G.e · Costa A.e

Author affiliations

aDepartment DISCAFF, University of East Piedmont ‘Amedeo Avogadro’, Novara, and bDepartment of Experimental Medicine, General Pathology Section, Genoa, Italy; cDepartment of Biochemistry, University of Alberta, Edmonton, Alta., Canada; dDepartment of Biomedical Sciences & Oncology and Department of Surgery, University of Turin, Turin, and eDepartment of Experimental Oncology, Istituto Nazionale per lo Studio e la Cura dei Tumori, Milan, Italy

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Oncology 2003;65:152–158

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Article / Publication Details

First-Page Preview
Abstract of Laboratory/Clinical Translational Research

Published online: August 29, 2003
Issue release date: August 2003

Number of Print Pages: 7
Number of Figures: 4
Number of Tables: 2

ISSN: 0030-2414 (Print)
eISSN: 1423-0232 (Online)

For additional information: http://www.karger.com/OCL

Abstract

Objective: Hepatic phosphatidylethanolamine is converted into phosphatidylcholine by the enzyme phosphatidylethanolamine N-methyltransferase (PEMT) when the dietary choline supply is inadequate. Our previous reports implicated PEMT in the regulation of hepatocyte growth and transformation. In the present study, we analyzed PEMT activity, Pempt gene status and its mRNA expression in 29 human hepatocellular carcinomas (HCC). Methods: The status of the Pempt gene and PEMT2 mRNA expression were evaluated with Southern and Northern blotting, respectively, in HCC and the noninvolved liver. PEMT activity was assessed by biochemical assay. Cell proliferation markers were defined by immunohistochemical or histoautoradiographic methods. Results: PEMT activity was lower in HCC than in the noninvolved liver and it was negligible in 62% of the tumors. No deletions or mutations of the Pempt gene were found and PEMT2 mRNA expression was absent or reduced in HCC compared with peritumoral liver tissue. PEMT2 mRNA expression was inversely related to tumor proliferation and to histologic grade. Patients whose HCC did not express PEMT2 mRNA showed poorer outcomes for cancer-related survival than those with PEMT2-positive HCC. Conclusions: The present findings suggest that (1) clones lacking PEMT2 expression may have been selected during liver tumorigenesis and progression, and (2) PEMT2 expression seems to be associated with clinical progression.

© 2003 S. Karger AG, Basel


Article / Publication Details

First-Page Preview
Abstract of Laboratory/Clinical Translational Research

Published online: August 29, 2003
Issue release date: August 2003

Number of Print Pages: 7
Number of Figures: 4
Number of Tables: 2

ISSN: 0030-2414 (Print)
eISSN: 1423-0232 (Online)

For additional information: http://www.karger.com/OCL


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