Overexpression of E2F-1 leads to bax-independent cell death in human glioma cells

dc.contributor.authorMitlianga, P. G.en
dc.contributor.authorGomez-Manzano, C.en
dc.contributor.authorKyritsis, A. P.en
dc.contributor.authorFueyo, J.en
dc.date.accessioned2015-11-24T19:00:26Z
dc.date.available2015-11-24T19:00:26Z
dc.identifier.issn1019-6439-
dc.identifier.urihttps://olympias.lib.uoi.gr/jspui/handle/123456789/19531
dc.rightsDefault Licence-
dc.subjectAdenoviridae/geneticsen
dc.subject*Apoptosisen
dc.subject*Cell Cycle Proteinsen
dc.subjectCell Survivalen
dc.subject*DNA-Binding Proteinsen
dc.subjectE2F Transcription Factorsen
dc.subjectE2F1 Transcription Factoren
dc.subject*Gene Therapyen
dc.subjectGlioma/chemistry/pathology/*therapyen
dc.subjectHumansen
dc.subjectProto-Oncogene Proteins/analysis/*genetics/physiologyen
dc.subject*Proto-Oncogene Proteins c-bcl-2en
dc.subjectTranscription Factors/analysis/*genetics/physiologyen
dc.subjectTumor Cells, Cultureden
dc.subjectbcl-2-Associated X Proteinen
dc.titleOverexpression of E2F-1 leads to bax-independent cell death in human glioma cellsen
heal.abstractGliomas are highly resistant to any kind of treatment. Multiple genetic abnormalities exist in gliomas indicating that effective gene therapy should be directed towards replacement of multiple rather than single genes. Bax is a protein of the Bcl-2 family that promotes apoptosis and functions as a tumor suppressor gene. The E2F family of transcription factors plays a pivotal role in the regulation of cell-cycle and cell-death related genes in gliomas. We examined the therapeutic potential of the simultaneous transfer of Bax and E2F molecules (1, 2 or 4) to gliomas. We used first generation E1A-deleted adenoviral vectors to transduce the E2Fs and Bax cDNAs. The recombinant adenoviral vector encoding bax uses the inducible Cre-loxP system to transduce the protein expression. Western blot analysis and immunofluorescence assays demonstrated high level of expression of the exogenous proteins. Trypan blue cell viability assays and flow cytometric cell-cycle analysis demonstrated an additive effect of these molecules to induce cell death via apoptosis. Western blot analysis showed that the ectopic expression of E2F-1 decreased the level of expression of Bax. These results indicate that E2F-1 and Bax have an additive anti-glioma effect when expressed simultaneously at high levels. Our data also suggest that Bax is not involved in the E2F-1-mediated apoptosis.en
heal.accesscampus-
heal.fullTextAvailabilityTRUE-
heal.identifier.secondaryhttp://www.ncbi.nlm.nih.gov/pubmed/12370749-
heal.journalNameInt J Oncolen
heal.journalTypepeer-reviewed-
heal.languageen-
heal.publicationDate2002-
heal.recordProviderΠανεπιστήμιο Ιωαννίνων. Σχολή Επιστημών Υγείας. Τμήμα Ιατρικήςel
heal.typejournalArticle-
heal.type.elΆρθρο Περιοδικούel
heal.type.enJournal articleen

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