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PPAR Research
Volume 2008 (2008), Article ID 250568, 7 pages
http://dx.doi.org/10.1155/2008/250568
Review Article

Chondrosarcoma and Peroxisome Proliferator-Activated Receptor

1Department of Human Morphology, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University, 2-5-1 Shikata-cho, Okayama 700-8558, Japan
2Department of Orthopaedic Surgery, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University, 2-5-1 Shikata-cho, Okayama 700-8558, Japan

Received 1 March 2008; Accepted 17 July 2008

Academic Editor: Dipak Panigrahy

Copyright © 2008 K. Nishida 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

Induction of differentiation and apoptosis in cancer cells by ligands of PPAR 𝛾 is a novel therapeutic approach to malignant tumors. Chondrosarcoma (malignant cartilage tumor) and OUMS-27 cells (cell line established from grade III human chondrosarcoma) express PPAR 𝛾 . PPAR 𝛾 ligands inhibited cell proliferation in a dose-dependent manner, and induced apoptosis of OUMS-27. The higher-grade chondrosarcoma expressed a higher amount of antiapoptotic Bcl-xL in vivo. The treatment of OUMS-27 by 15d-PG J 2 , the most potent endogenous ligand for PPAR 𝛾 , downregulated expression of Bcl-xL and induced transient upregulation of proapoptotic Bax, which could accelerate cytochrome c release from mitochondria to the cytosol, followed by induction of caspase-dependent apoptosis. 15d-PG J 2 induced the expression of CDK inhibitor p21 protein in human chondrosarcoma cells, which appears to be involved in the mechanism of inhibition of cell proliferation. These findings suggest that targeted therapy with PPAR 𝛾 ligands could be a novel strategy against chondrosarcoma.