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PPAR Research
Volume 2008, Article ID 209520, 4 pages
http://dx.doi.org/10.1155/2008/209520
Review Article

The Role of PPAR 𝜸 in Hepatocellular Carcinoma

Gastroenterology Unit, Cliniques universitaires Saint-Luc, Université catholique de Louvain, Avenue Hippocrate 10, 1200 Bruxelles, Belgium

Received 10 March 2008; Accepted 14 May 2008

Academic Editor: Dipak Panigrahy

Copyright © 2008 Ivan Borbath and Yves Horsmans. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

Abstract

Hepatocellular carcinoma (HCC) is the third leading cause of cancer-related death worldwide. This cancer develops mainly in cirrhotic patients. The cirrhotic liver is considered to be a preneoplastic organ, suggesting the rationale for cancer prevention. PPAR 𝛾 is a nuclear transcription factor whose activation leads to interaction in the metabolism of lipids, insulin sensitization of peripheral cells, anti-inflammatory action. It can also induce differentiation and inhibits proliferation of cancer cells. Until now, data using PPAR 𝛾 ligands in HCC have demonstrated mainly in in vitro models that its activation could be due to an antiproliferative effect. PPAR 𝛾 ligand administration has also been associated with a diminution of liver fibrosis in animal models, and potentially also on tumoral cell death. Soma data show that the favorable effect of natural and synthetized PPAR 𝛾 agonists could also be independent of PPAR 𝛾 activation. Furthermore, in some situations, PPAR 𝛾 antagonists have also an anticancer effect. Therefore, we can conclude that the link between activation of the PPAR 𝛾 pathway and an anticancer activity is suggested but until now not firmly established in HCC.