Affiliation:
1. Gastroenterology Unit, Cliniques universitaires Saint-Luc, Université catholique de Louvain, Avenue Hippocrate 10, 1200 Bruxelles, Belgium
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 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 ligands in HCC have demonstrated mainly in in vitro models that its activation could be due to an antiproliferative effect. PPAR 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 agonists could also be independent of PPAR activation. Furthermore, in some situations, PPAR antagonists have also an anticancer effect. Therefore, we can conclude that the link between activation of the PPAR pathway and an anticancer activity is suggested but until now not firmly established in HCC.
Subject
Pharmacology (medical),Drug Discovery
Cited by
23 articles.
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