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Anti- and Protumorigenic Effects of PPARγin Lung Cancer Progression: A Double-Edged Sword
Author(s) -
Howard Li,
Mary C.M. WeiserEvans,
Raphael A. Nemenoff
Publication year - 2012
Publication title -
ppar research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.164
H-Index - 49
eISSN - 1687-4765
pISSN - 1687-4757
DOI - 10.1155/2012/362085
Subject(s) - peroxisome proliferator activated receptor , carcinogenesis , proinflammatory cytokine , cancer research , nuclear receptor , oncogene , transcription factor , tumor promotion , thiazolidinedione , receptor , cancer , lung cancer , biology , medicine , bioinformatics , inflammation , immunology , gene , biochemistry , endocrinology , cell cycle , type 2 diabetes , diabetes mellitus
Peroxisome proliferator-activated receptor- γ (PPAR γ ) 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 PPAR γ include naturally occurring fatty acids and the thiazolidinedione class of antidiabetic drugs. Activation of PPAR γ 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 PPAR γ has been reported to be protumorigenic in some in vitro systems and in vivo models. Here, we review the available data that implicate PPAR γ in lung carcinogenesis and highlight the challenges of targeting PPAR γ in lung cancer treatments.

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