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(American Journal of Pathology. 2007;170:722-732.)
© 2007 American Society for Investigative Pathology
DOI: 10.2353/ajpath.2007.060651

Activation of Peroxisome Proliferator-Activated Receptor {gamma} Contributes to the Survival of T Lymphoma Cells by Affecting Cellular Metabolism

Chunyan Yang, Seung-Hee Jo, Balazs Csernus, Elizabeth Hyjek, Yifang Liu, Amy Chadburn and Y. Lynn Wang

From the Department of Pathology and Laboratory Medicine, Weill Medical College of Cornell University, New York, New York

Peroxisome proliferator-activated receptor {gamma} (PPAR{gamma}) is a metabolic regulator involved in maintaining glucose and fatty acid homeostasis. Besides its metabolic functions, the receptor has also been implicated in tumorigenesis. Ligands of PPAR{gamma} induce apoptosis in several types of tumor cells, leading to the proposal that these ligands may be used as antineoplastic agents. However, apoptosis induction requires high doses of ligands, suggesting the effect may not be receptor-dependent. In this report, we show that PPAR{gamma} is expressed in human primary T-cell lymphoma tissues and activation of PPAR{gamma} with low doses of ligands protects lymphoma cells from serum starvation-induced apoptosis. The prosurvival effect of PPAR{gamma} was linked to its actions on cellular metabolic activities. In serum-deprived cells, PPAR{gamma} attenuated the decline in ATP, reduced mitochondrial hyperpolarization, and limited the amount of reactive oxygen species (ROS) in favor of cell survival. Moreover, PPAR{gamma} regulated ROS through coordinated transcriptional control of a set of proteins and enzymes involved in ROS metabolism. Our study identified cell survival promotion as a novel activity of PPAR{gamma}. These findings highlight the need for further investigation into the role of PPAR{gamma} in cancer before widespread use of its agonists as anticancer therapeutics.




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