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dc.contributor.authorBrown, James E. P.
dc.contributor.authorDarling, John L.
dc.contributor.authorDunmore, Simon J.
dc.contributor.authorBassey, S.
dc.date.accessioned2008-06-12T08:30:38Z
dc.date.available2008-06-12T08:30:38Z
dc.date.issued2005
dc.identifier.citationNeuro-oncology, 7(3): 296
dc.identifier.issn1522-8517
dc.identifier.urihttp://hdl.handle.net/2436/29933
dc.descriptionAbstracts from Neuro-Oncology are provided here courtesy of Society for Neuro-Oncology and Duke University Press
dc.description.abstractRecent studies have suggested that the glitazones, a group of PPAR agonists commonly prescribed as therapy in type 2 diabetes, could have a role in regulation of cell viability in astrocytomas and glioma cell lines, possibly due to a modulation of reactive oxygen species (ROS) production. PPAR agonists are also known to regulate expression of the mitochondrial protein UCP-2, and UCP-2 has a purported role in ROS regulation amongst others. This study investigated the expression of UCP-2 in U251MG glioma cells and its regulation by PPAR agonists. U251MG glioma cells were cultured according to standard methods and treated with PPAR alpha, delta, and gamma agonists (10 μM WY14643, 10 nM PGI2, 10 μM rosiglitazone and 10 nM PGJ2, respectively) for 24 h. Total RNA was subsequently extracted and semiquantitative RT-PCR used to evaluate UCP-2 mRNA expression. Results showed that UCP-2 was expressed in all control and treatment samples and that its expression was regulated differentially by the various PPAR receptor subtype agonists tested. This novel finding that UCP-2 is expressed in glioma cells, and that its expression is regulated by PPAR agonists, suggests a potential mechanism for the cytotoxic effects of glitazones that have been previously reported, and describes a mechanism which could possibly be manipulated as a potential therapeutic avenue in the future.
dc.language.isoen
dc.publisherSociety for Neuro-Oncology and Duke University Press
dc.relation.urlhttp://www.pubmedcentral.nih.gov/articlerender.fcgi?artid=1871910
dc.subjectCancer genetics
dc.subjectBrain Tumours
dc.subjectChemotherapeutic targets
dc.subjectMalignant Tumours
dc.subjectGlioma
dc.subjectU251MG
dc.subjectRNA
dc.subjectPPAR agonists
dc.subjectUCP-2
dc.subjectAstrogliomas
dc.subjectReactive Oxygen Species
dc.subjectGlitazones
dc.subjectAstrocytoma
dc.subjectOncology
dc.subject.meshCell Line, Tumor
dc.titleRegulation of uncoupling protein-2 (UCP-2) expression in human glioma cells by peroxisome proliferators-activated receptor (PPAR) agonists
dc.title.alternativeIn: Abstracts from the World Federation of Neuro-Oncology 2nd Quadrennial Meeting and the 6th Meeting of the European Association for Neuro-Oncology, May 5–8, 2005, Edinburgh, UK. No.56
dc.typeConference contribution
dc.identifier.journalNeuro-oncology
html.description.abstractRecent studies have suggested that the glitazones, a group of PPAR agonists commonly prescribed as therapy in type 2 diabetes, could have a role in regulation of cell viability in astrocytomas and glioma cell lines, possibly due to a modulation of reactive oxygen species (ROS) production. PPAR agonists are also known to regulate expression of the mitochondrial protein UCP-2, and UCP-2 has a purported role in ROS regulation amongst others. This study investigated the expression of UCP-2 in U251MG glioma cells and its regulation by PPAR agonists. U251MG glioma cells were cultured according to standard methods and treated with PPAR alpha, delta, and gamma agonists (10 μM WY14643, 10 nM PGI2, 10 μM rosiglitazone and 10 nM PGJ2, respectively) for 24 h. Total RNA was subsequently extracted and semiquantitative RT-PCR used to evaluate UCP-2 mRNA expression. Results showed that UCP-2 was expressed in all control and treatment samples and that its expression was regulated differentially by the various PPAR receptor subtype agonists tested. This novel finding that UCP-2 is expressed in glioma cells, and that its expression is regulated by PPAR agonists, suggests a potential mechanism for the cytotoxic effects of glitazones that have been previously reported, and describes a mechanism which could possibly be manipulated as a potential therapeutic avenue in the future.


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