PPARand Apoptosis in Cancer
Open Access
- 1 January 2008
- journal article
- review article
- Published by Hindawi Limited in PPAR Research
- Vol. 2008, 1-12
- https://doi.org/10.1155/2008/704165
Abstract
Peroxisome proliferator-activated receptors (PPARs) are ligand binding transcription factors which function in many physiological roles including lipid metabolism, cell growth, differentiation, and apoptosis. PPARs and their ligands have been shown to play a role in cancer. In particular, PPARligands including endogenous prostaglandins and the synthetic thiazolidinediones (TZDs) can induce apoptosis of cancer cells with antitumor activity. Thus, PPARligands have a potential in both chemoprevention and therapy of several types of cancer either as single agents or in combination with other antitumor agents. Accordingly, the involvement of PPARand its ligands in regulation of apoptosis of cancer cells have been extensively studied. Depending on cell types or ligands, induction of apoptosis in cancer cells by PPARligands can be either PPAR-dependent or -independent. Through increasing our understanding of the mechanisms of PPARligand-induced apoptosis, we can develop better strategies which may include combining other antitumor agents for PPAR-targeted cancer chemoprevention and therapy. This review will highlight recent research advances on PPARand apoptosis in cancer.
Keywords
Funding Information
- Georgia Cancer Coalition (W81XWH-04-1-0142, P50 CA128613-01)
This publication has 85 references indexed in Scilit:
- Synergy between PPARγ Ligands and Platinum-Based Drugs in CancerCancer Cell, 2007
- Present concepts and future outlook: Function of peroxisome proliferator‐activated receptors (PPARs) for pathogenesis, progression, and therapy of cancerJournal of Cellular Physiology, 2007
- PPARγ inhibitors reduce tubulin protein levels by a PPARγ, PPARδ and proteasome‐independent mechanism, resulting in cell cycle arrest, apoptosis and reduced metastasis of colorectal carcinoma cellsInternational Journal of Cancer, 2006
- PPARγ is a key target of butyrate-induced caspase-3 activation in the colorectal cancer cell line Caco-2Apoptosis, 2006
- Troglitazone sensitizes tumor cells to TRAIL-induced apoptosis via down-regulation of FLIP and SurvivinApoptosis, 2006
- PPARγ insufficiency promotes follicular thyroid carcinogenesis via activation of the nuclear factor-κB signaling pathwayOncogene, 2005
- Inhibitors of the Arachidonic Acid Pathway and Peroxisome Proliferator–Activated Receptor Ligands Have Superadditive Effects on Lung Cancer Growth InhibitionCancer Research, 2005
- GW9662, a potent antagonist of PPARγ, inhibits growth of breast tumour cells and promotes the anticancer effects of the PPARγ agonist rosiglitazone, independently of PPARγ activationBritish Journal of Pharmacology, 2004
- Ligands of peroxisome proliferator-activated receptor γ induce apoptosis in multiple myelomaAnti-Cancer Drugs, 2004
- Peroxisome Proliferator-Activated Receptor γ Induces Pancreatic Cancer Cell ApoptosisBiochemical and Biophysical Research Communications, 2001