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Peroxisome Proliferator-Activated Receptor- Agonist Rosiglitazone– Induced Apoptosis in Leukemia K562 Cells and Its Mechanisms of Action

From the Third Hospital of Sun Yat-Sen University, Guangzhou, P. R. China

Correspondence: Please address correspondence to Dong-Jun Lin, Department of Hematology, the Third Affiliated Hospital of Sun Yat-sen University, Guangzhou, 510630, P. R. China; e-mail:lindongjun0168{at}163.com.

This study investigates the ability of a synthetic PPAR- agonist, rosiglitazone (RGZ), to induce apoptosis in leukemia K562 cells. The results revealed that RGZ (>40 mmol/L) inhibits the growth of K562 cells and causes apoptosis in a time and dose-dependent manner. Apoptosis is observed clearly by Hoechst 33258 staining. Western blotting analysis demonstrates the cleavage of caspase-3 zymogen protein with the appearance of its 17-kD subunit and a dose-dependent cleavage of poly (ADP-ribose) polymerase. Furthermore, RGZ treatment down-regulates anti-apoptotic protein Bcl-2 and up-regulates pro-apoptotic protein Bax in a dosedependent manner after the cells are treated for 48 hours. Telomerase activity is decreased concurrently in a dosedependent manner. We therefore conclude that RGZ induces apoptosis in K562 cells in vitro, and that RGZ-induced apoptosis in K562 cells is highly correlated with activation of caspase-3, decreasing telomerase activity, down-regulation of the anti-apoptotic protein Bcl-2, and up-regulation of the pro-apoptotic protein Bax.

Key Words: rosiglitazone (RGZ) • apoptosis • leukemia

International Journal of Toxicology, Vol. 28, No. 2, 123-131 (2009)
DOI: 10.1177/1091581809335312


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