activated ppar targets surface and intracellular signals that inhibit the proliferation of lung carcinoma cells激活ppar目标表面和胞内信号,抑制肺癌细胞的增殖.pdfVIP
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activated ppar targets surface and intracellular signals that inhibit the proliferation of lung carcinoma cells激活ppar目标表面和胞内信号,抑制肺癌细胞的增殖
Hindawi Publishing Corporation
PPAR Research
Volume 2008, Article ID 254108, 8 pages
doi:10.1155/2008/254108
Review Article
Activated PPARγ Targets Surface and Intracellular Signals That
Inhibit the Proliferation of Lung Carcinoma Cells
Shou Wei Han1 and Jesse Roman1, 2
1 Division of Pulmonary, Allergy and Critical Care Medicine, Department of Medicine, Emory University School of Medicine,
615 Michael Street Suite 205, Atlanta, GA 30322, USA
2 Atlanta VA Medical Center, Department of Medicine, 1670 Clairmont Road, Decatur, GA 30033, USA
Correspondence should be addressed to Shou Wei Han, shan2@
Received 28 April 2008; Accepted 24 June 2008
Recommended by Dipak Panigrahy
Peroxisome proliferator-activated receptors (PPARs) are ligand-activated transcription factors belonging to the nuclear hormone
receptor superfamily. Their discovery in the 1990s provided insights into the cellular mechanisms involved in the control of energy
homeostasis, the regulation of cell differentiation, proliferation, and apoptosis, and the modulation of important biological and
pathological processes related to inflammation and cancer biology, among others. Since then, PPARs have become an exciting
target for the development of therapies directed at many disorders including cancer. PPARs are expressed in many tumors including
lung cancer, and their function has been linked to the process of carcinogenesis. Consequently, intense research is being conducted
in this area with the hope of discovering new PPAR-related therapeutic targets for the treatment of lung cancer. This review
summarizes the research being conducted in this area, and focuses on the mechanisms by which a member of this family (PPARγ)
is believed to affect lung tumor cell biology.
Copyright © 2008 S. W
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