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Carcinogenesis Advance Access published online on January 20, 2005
Carcinogenesis, doi:10.1093/carcin/bgi022
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Oxford University Press
Received September 30, 2004
Revised December 13, 2004
Accepted January 8, 2005

CANCER BIOLOGY

Prostaglandin E2 promotes migration and adhesion in hepatocellular carcinoma cells

Rafael Mayoral 1, Amalia Fernández-Martínez 1, Lisardo Boscá 1, and Paloma Martín-Sanz 1*

1 Instituto de Bioquímica, Centro Mixto CSIC-UCM, Facultad de Farmacia, Universidad Complutense, 28040 Madrid, Spain; Centro Nacional de Investigaciones Cardiovasculares, Facultad de Farmacia, Universidad Complutense, 28040 Madrid, Spain

* To whom correspondence should be addressed.
Paloma Martín-Sanz, E-mail: pmartin{at}farm.ucm.es


  Abstract

The effect of the expression of cyclooxygenase-2 (COX-2) and prostaglandin E2 (PGE2) synthesis on cell migration, matrix metalloproteinases secretion and adhesion of human hepatoma cell lines has been investigated. A close correlation was observed between the expression of COX-2 under basal conditions and the secretion of matrix metalloproteinases 2 and 9. Cell migration in HuH-7 cells, which express high constitutive levels of COX-2, was significantly inhibited by selective inhibitors of COX-2, and enhanced by exogenous addition of PGE2. Hepatocellular carcinoma cells expressed {beta}1 and {alpha}V{beta}3 integrins, exhibiting an increase in cell adhesion onto fibronectin and vitronectin. Moreover, addition of PGE2 increased {beta}1 integrin levels and adhesion on vitronectin in HuH-7 cells. Inhibitors of MEK/ERK, p38 MAPK, protein kinase A and protein kinase C impaired the migration of HuH-7 cells induced by PGE2, indicating the involvement of multiple pathways in the process. Taken together these results support the existence of a relationship between COX-2-derived PGE2 synthesis and migration and adhesion through an integrin-dependent pathway in hepatocellular carcinoma cells.


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