The PPARgamma Agonist Rosiglitazone Inhibits Glioma Cell Proliferation and Migration in vitro and Glioma Tumor Growth in vivo.
- Author:
Chang Hwa CHOI
1
;
Chae Hwa KWON
;
Yong Keun KIM
Author Information
- Publication Type:In Vitro ; Original Article
- Keywords: PPARgamma; rosiglitazone; proliferation; migration; glioma tumor growth; apoptosis; MMP-9; human U87MG glioma cells
- MeSH: Administration, Oral; Animals; Apoptosis; Cell Death; Cell Movement; Cell Proliferation; Glioma; Humans; Peroxisomes; PPAR gamma; RNA, Messenger; Thiazolidinediones; Tumor Burden
- From:Experimental Neurobiology 2009;18(2):112-122
- CountryRepublic of Korea
- Language:English
- Abstract: Peroxisome proliferator-activated receptor-gamma (PPARgamma) has been implicated in the growth inhibition of a number of cancer cells. In the present study, we investigated the antitumor effect of the PPARgamma 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.
