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PPAR Research
Volume 2012, Article ID 362085, 12 pages
http://dx.doi.org/10.1155/2012/362085
Review Article

Anti- and Protumorigenic Effects of PPARγ in Lung Cancer Progression: A Double-Edged Sword

1Division of Pulmonary Sciences and Critical Care Medicine, Department of Medicine, University of Colorado Denver, Aurora, CO 80045, USA
2Pulmonary and Critical Care Section, Department of Medicine, Denver Veterans Affairs Medical Center, Denver, CO 80220, USA
3Division of Renal Diseases and Hypertension, Department of Medicine, University of Colorado Denver, Aurora, CO 80045, USA
4Division of Renal Diseases and Hypertension, Department of Medicine, University of Colorado, Anschutz Medical Campus, C-281 12700 East 19th Avenue, Aurora, CO 80045, USA

Received 29 February 2012; Accepted 9 July 2012

Academic Editor: Andrea Galli

Copyright © 2012 Howard Li et al. 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

Peroxisome proliferator-activated receptor-γ (PPARγ) is a member of the nuclear receptor superfamily of ligand-activated transcription factors that plays an important role in the control of gene expression linked to a variety of physiological processes, including cancer. Ligands for PPARγ include naturally occurring fatty acids and the thiazolidinedione class of antidiabetic drugs. Activation of PPARγ in a variety of cancer cells leads to inhibition of growth, decreased invasiveness, reduced production of proinflammatory cytokines, and promotion of a more differentiated phenotype. However, systemic activation of PPARγ has been reported to be protumorigenic in some in vitro systems and in vivo models. Here, we review the available data that implicate PPARγ in lung carcinogenesis and highlight the challenges of targeting PPARγ in lung cancer treatments.