Exp Neurobiol.  2009 Dec;18(2):112-122. 10.5607/en.2009.18.2.112.

The PPARgamma Agonist Rosiglitazone Inhibits Glioma Cell Proliferation and Migration in vitro and Glioma Tumor Growth in vivo

Affiliations
  • 1Department of Neurosurgery, Pusan National University College of Medicine, Busan 602-739, Korea.
  • 2Department of Physiology, Pusan National University College of Medicine, Busan 602-739, Korea. kim430@pusan.ac.kr

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.

Keyword

PPARgamma; rosiglitazone; proliferation; migration; glioma tumor growth; apoptosis; MMP-9; human U87MG glioma cells

MeSH Terms

Administration, Oral
Animals
Apoptosis
Cell Death
Cell Movement
Cell Proliferation
Glioma
Humans
Peroxisomes
PPAR gamma
RNA, Messenger
Thiazolidinediones
Tumor Burden
PPAR gamma
RNA, Messenger
Thiazolidinediones
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