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Peroxisome Proliferator-Activated Receptor γ and Lung Cancer Biology
  1. Jesse Roman, MD
  1. From the Department of Medicine, Division of Pulmonary, Allergy and Critical Care Medicine, Emory University School of Medicine; and The Atlanta Veterans Affairs Medical Center Atlanta, GA.
  1. Supported by grants from the National Institutes of Health and the Veterans Affairs Research Service.
  2. Reprints: Jesse Roman, MD, Emory Division of Pulmonary, Allergy and Critical Care Medicine, Whitehead Biomedical Research Building, 615 Michael St, Room 205-M, Atlanta, GA 30322. E-mail: jroman{at}emory.edu.

Implications for Therapy

Abstract

Peroxisome proliferator-activated receptors (PPARs) are members of the nuclear receptor family of transcriptional modulators. In addition to their known roles in regulation of metabolism and inflammation, PPARs have also been implicated in carcinogenesis based on studies showing their ability to modulate cellular differentiation, proliferation, and apoptosis. Of the 3 PPARs identified to date (PPARα, PPARβ/δ, and PPARγ), PPARγ has been studied the most in part because of the availability of PPARγ agonists (also known as PPARγ ligands). In many tumor cells, including lung carcinoma cells, activation of PPARγ results in decreased cellular proliferation; this is particularly true for non-small cell lung carcinoma, the most common malignant lung tumor in the United States. Studies performed in xenograft models of lung cancer also show decreased tumor growth and progression in animals treated with PPARγ ligands. More recently, data are emerging from retrospective clinical studies that suggest a protective role for PPARγ ligands on the incidence of lung cancer. This review summarizes the available data that implicate PPARs in lung carcinogenesis while focusing on PPARγ as a potential target for the development of novel anti-lung cancer treatment strategies.

Key Words
  • carcinogenesis
  • tumor
  • PPAR
  • proliferation
  • signaling
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