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Please use this identifier to cite or link to this item: https://olympias.lib.uoi.gr/jspui/handle/123456789/21009
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dc.contributor.authorPuduvalli, V. K.en
dc.contributor.authorSampath, D.en
dc.contributor.authorBruner, J. M.en
dc.contributor.authorNangia, J.en
dc.contributor.authorXu, R.en
dc.contributor.authorKyritsis, A. P.en
dc.date.accessioned2015-11-24T19:12:03Z-
dc.date.available2015-11-24T19:12:03Z-
dc.identifier.issn1360-8185-
dc.identifier.urihttps://olympias.lib.uoi.gr/jspui/handle/123456789/21009-
dc.rightsDefault Licence-
dc.subject*Apoptosisen
dc.subjectApoptosis Regulatory Proteinsen
dc.subjectCell Line, Tumoren
dc.subjectEnzyme Activationen
dc.subjectGlioma/*pathologyen
dc.subjectHumansen
dc.subjectJNK Mitogen-Activated Protein Kinases/*metabolismen
dc.subjectMAP Kinase Kinase 4en
dc.subjectMembrane Glycoproteins/*physiologyen
dc.subjectMitogen-Activated Protein Kinase Kinases/*metabolismen
dc.subjectProtein-Serine-Threonine Kinases/*antagonists & inhibitorsen
dc.subjectProto-Oncogene Proteins/*antagonists & inhibitorsen
dc.subjectProto-Oncogene Proteins c-akten
dc.subjectSignal Transductionen
dc.subjectTNF-Related Apoptosis-Inducing Liganden
dc.subjectTumor Necrosis Factor-alpha/*physiologyen
dc.titleTRAIL-induced apoptosis in gliomas is enhanced by Akt-inhibition and is independent of JNK activationen
heal.typejournalArticle-
heal.type.enJournal articleen
heal.type.elΆρθρο Περιοδικούel
heal.identifier.primary10.1007/s10495-005-6078-3-
heal.identifier.secondaryhttp://www.ncbi.nlm.nih.gov/pubmed/15711939-
heal.identifier.secondaryhttp://www.springerlink.com/content/v514l54633t42674/fulltext.pdf-
heal.languageen-
heal.accesscampus-
heal.recordProviderΠανεπιστήμιο Ιωαννίνων. Σχολή Επιστημών Υγείας. Τμήμα Ιατρικήςel
heal.publicationDate2005-
heal.abstractPatients with malignant gliomas have a poor prognosis and new treatment paradigms are needed against this disease. TRAIL/Apo2L selectively induces apoptosis in malignant cells sparing normal cells and is hence of interest as a potential therapeutic agent against gliomas. To determine the factors that modulate sensitivity to TRAIL, we examined the differences in TRAIL-activated signaling pathways in glioma cells with variable sensitivities to the agent. Apoptosis in response to TRAIL was unrelated to DR5 expression or endogenous p53 status in a panel of 8 glioma cell lines. TRAIL activated the extrinsic (cleavage of caspase-8, caspase-3 and PARP) and mitochondrial apoptotic pathways and reduced FLIP levels. It also induced caspase-dependent JNK activation, which did not influence TRAIL-induced apoptosis. Because the pro-survival PI3K/Akt pathway is highly relevant to gliomas, we assessed whether Akt could protect against TRAIL-induced apoptosis. Pretreatment with SH-6, a novel Akt inhibitor, enhanced TRAIL-induced apoptosis, suggesting a protective role for Akt. Conversely, TRAIL induced caspase-dependent cleavage of Akt neutralizing its anti-apoptotic effects. These results demonstrate that TRAIL-induced apoptosis in gliomas involves both activation of death pathways and downregulation of survival pathways. Additional studies are warranted to determine the therapeutic potential of TRAIL against gliomas.en
heal.journalNameApoptosisen
heal.journalTypepeer-reviewed-
heal.fullTextAvailabilityTRUE-
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