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Carcinogenesis Advance Access originally published online on January 20, 2005
Carcinogenesis 2005 26(4):753-761; doi:10.1093/carcin/bgi022
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Carcinogenesis vol.26 no.4 © Oxford University Press 2005; all rights reserved.

ARTICLE

Prostaglandin E2 promotes migration and adhesion in hepatocellular carcinoma cells

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

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

* To whom correspondence should be addressed. Tel: +349 1394 1853; Fax: +349 1394 1782; Email: pmartin{at}farm.ucm.es

The effect of the expression of cyclooxygenase-2 (COX-2) and prostaglandin E2 (PGE2) synthesis on cell migration, the secretion of matrix metalloproteinases (MMPs) and the 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 MMP-2 and MMP-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 (HCC) cells expressed ß1 and {alpha}Vß3 integrins, exhibiting an increase in cell adhesion onto fibronectin and vitronectin. Moreover, addition of PGE2 increased the ß1 integrin levels and adhesion on vitronectin in HuH-7 cells. Inhibitors of MEK/ERK, p38 MAPK, protein kinases A and 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 HCC cells.


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