Exp Neurobiol 2009; 18(2): 112-122
Published online December 31, 2009
© The Korean Society for Brain and Neural Sciences
Chang Hwa Choi1, Chae Hwa Kwon2 and Yong Keun Kim2*
Departments of 1Neurosurgery and 2Physiology, Pusan National University College of Medicine, Busan 602-739, Korea
Correspondence to: *To whom correspondence should be addressed.
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Peroxisome proliferator-activated receptor-Ճ (PPARՃ) has been implicated in the growth inhibition of a number of cancer cells. In the present study, we investigated the antitumor effect of the PPARՃ agonist rosiglitazone in U87MG human glioma cells. Rosiglitazone treatment in vitro reduced cell proliferation without induction of cell death in a dose- and time-dependent manner. Rosiglitazone decreased cell migration and mRNA level of MMP-9. Rosiglitazone treatment also induced marked changes in glioma cell morphology. Oral administration of rosiglitazone in animals with subcutaneous U87MG glioma cells reduced tumor volume. Subsequent tumor tissue analysis showed that rosiglitazone decreased the number of PCNA-positive staining cells and MMP-9 expression and induced apoptosis of tumor cells. These data suggest that rosiglitazone exerts antineoplastic effect in U87MG cells and may serve as potential therapeutic agent for malignant human gliomas.
Keywords: PPARՃ,, rosiglitazone, proliferation, migration, glioma tumor growth, apoptosis, MMP-9, human U87MG glioma cells