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PPAR Research
Volume 2008, Article ID 704165, 12 pages
Review Article

PPAR 𝛾 and Apoptosis in Cancer

Department of Hematology and Medical Oncology, Winship Cancer Institute, Emory University School of Medicine, Atlanta, GA 30322, USA

Received 19 February 2008; Revised 21 April 2008; Accepted 11 June 2008

Academic Editor: Dipak Panigrahy

Copyright © 2008 Heath A. Elrod and Shi-Yong Sun. 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.


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, PPAR 𝛾 ligands including endogenous prostaglandins and the synthetic thiazolidinediones (TZDs) can induce apoptosis of cancer cells with antitumor activity. Thus, PPAR 𝛾 ligands 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 PPAR 𝛾 and 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 PPAR 𝛾 ligands can be either PPAR 𝛾 -dependent or -independent. Through increasing our understanding of the mechanisms of PPAR 𝛾 ligand-induced apoptosis, we can develop better strategies which may include combining other antitumor agents for PPAR 𝛾 -targeted cancer chemoprevention and therapy. This review will highlight recent research advances on PPAR 𝛾 and apoptosis in cancer.