v-FBR-fos oncogene fails to rescue mammalian cells from growth arrest but affects the responses of human fibroblasts to heparin

dc.contributor.authorKolettas, E.en
dc.contributor.authorEvangelou, A.en
dc.contributor.authorGonos, E. S.en
dc.date.accessioned2015-11-24T18:49:38Z
dc.date.available2015-11-24T18:49:38Z
dc.identifier.issn0250-7005-
dc.identifier.urihttps://olympias.lib.uoi.gr/jspui/handle/123456789/17988
dc.rightsDefault Licence-
dc.subjectAnimalsen
dc.subject*Cell Agingen
dc.subjectCell Divisionen
dc.subjectCell Lineen
dc.subjectCell Line, Transformeden
dc.subject*Cell Transformation, Viralen
dc.subjectFibroblasts/*metabolismen
dc.subjectHeparin/*pharmacologyen
dc.subjectHumansen
dc.subjectMesoderm/cytologyen
dc.subjectOncogene Proteins v-fos/biosynthesis/genetics/*physiologyen
dc.subjectProto-Oncogene Proteins c-jun/biosynthesis/geneticsen
dc.subjectRNA, Messenger/biosynthesisen
dc.subjectRatsen
dc.subject*Sarcoma Viruses, Murineen
dc.subjectTransfectionen
dc.titlev-FBR-fos oncogene fails to rescue mammalian cells from growth arrest but affects the responses of human fibroblasts to heparinen
heal.abstractThe effects of v-fos oncogene on the proliferation of mammalian cells were studied using several approaches. Constitutive overexpression of v-FBR-fos in normal human fibroblasts (MRC-5) and of v-FBR-fos in human chondrocytes (HAC21) failed to immortalise them, extend their in vitro lifespan, increase their growth rates or induce cellular transformation. Further, v-FBR-fos did not render MRC-5 growth factor-independent or alter their responsivenness to serum, but it markedly suppressed their heparin-induced proliferation. A conditionally immortalized, temperature-sensitive rat embryo fibroblast cell line (tsa14) which undergoes growth arrest upon inactivation of a thermolabile SV40 large T antigen by a temperature shift producing a phenotype that mimmicks the senescent phenotype, was also used to study the effects of v-FBR-fos on cell proliferation. Whereas a wild-type SV40 large T antigen rescued tsa14 from a temperature-dependent growth arrest, v-FBR-fos failed to do so. Hence, v-FBR-fos was not sufficient to, at least, complement the tsa14 growth defect. There was no change in the expression of c-jun and junB, members of the AP-1 transcriptional complex in MRC-5v-fos cells. These data show that v-FBR-fos is not sufficient to rescue mammalian cells from senescence but it can affect the responses of human fibroblasts to heparin suggesting a role of fos in cell proliferation.en
heal.accesscampus-
heal.fullTextAvailabilityTRUE-
heal.identifier.secondaryhttp://www.ncbi.nlm.nih.gov/pubmed/11299775-
heal.journalNameAnticancer Resen
heal.journalTypepeer-reviewed-
heal.languageen-
heal.publicationDate2001-
heal.recordProviderΠανεπιστήμιο Ιωαννίνων. Σχολή Επιστημών Υγείας. Τμήμα Ιατρικήςel
heal.typejournalArticle-
heal.type.elΆρθρο Περιοδικούel
heal.type.enJournal articleen

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