Regulation of uncoupling protein-2 (UCP-2) expression in human glioma cells by peroxisome proliferators-activated receptor (PPAR) agonists

2.50
Hdl Handle:
http://hdl.handle.net/2436/29933
Title:
Regulation of uncoupling protein-2 (UCP-2) expression in human glioma cells by peroxisome proliferators-activated receptor (PPAR) agonists
Authors:
Brown, James E. P.; Darling, John L.; Dunmore, Simon J.; Bassey, S.
Other Titles:
In: 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
Abstract:
Recent 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.
Citation:
Neuro-oncology, 7(3): 296
Publisher:
Society for Neuro-Oncology and Duke University Press
Journal:
Neuro-oncology
Issue Date:
2005
URI:
http://hdl.handle.net/2436/29933
Additional Links:
http://www.pubmedcentral.nih.gov/articlerender.fcgi?artid=1871910
Type:
Meetings & Proceedings
Language:
en
Description:
Abstracts from Neuro-Oncology are provided here courtesy of Society for Neuro-Oncology and Duke University Press
ISSN:
1522-8517
Appears in Collections:
Cancer Research Group

Full metadata record

DC FieldValue Language
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): 296en
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 Pressen
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.en
dc.language.isoenen
dc.publisherSociety for Neuro-Oncology and Duke University Pressen
dc.relation.urlhttp://www.pubmedcentral.nih.gov/articlerender.fcgi?artid=1871910en
dc.subjectCancer geneticsen
dc.subjectBrain Tumoursen
dc.subjectChemotherapeutic targetsen
dc.subjectMalignant Tumoursen
dc.subjectGliomaen
dc.subjectU251MGen
dc.subjectRNAen
dc.subjectPPAR agonistsen
dc.subjectUCP-2en
dc.subjectAstrogliomasen
dc.subjectReactive Oxygen Speciesen
dc.subjectGlitazonesen
dc.subjectAstrocytomaen
dc.subjectOncologyen
dc.subject.meshCell Line, Tumoren
dc.titleRegulation of uncoupling protein-2 (UCP-2) expression in human glioma cells by peroxisome proliferators-activated receptor (PPAR) agonistsen
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.56en
dc.typeMeetings & Proceedingsen
dc.identifier.journalNeuro-oncologyen
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