Aven blocks DNA damage-induced apoptosis by stabilising Bcl-xL

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dc.contributor.authorKütük, Özgür
dc.contributor.authorBaşağa, Hüveyda
dc.contributor.buuauthorTemel, Şehime Gülsün
dc.contributor.buuauthorTolunay, Şahsine
dc.contributor.departmentUludağ Üniversitesi/Tıp Fakültesi/Tıbbi Genetik Anabilim Dalı.tr_TR
dc.contributor.departmentUludağ Üniversitesi/Tıp Fakültesi/Patoloji Anabilim Dalı.tr_TR
dc.contributor.researcheridAAG-8385-2021tr_TR
dc.contributor.researcheridAAI-1612-2021tr_TR
dc.contributor.scopusid6507885442tr_TR
dc.contributor.scopusid6602604390tr_TR
dc.date.accessioned2021-12-08T07:16:09Z
dc.date.available2021-12-08T07:16:09Z
dc.date.issued2010-09
dc.description.abstractInduction of apoptosis by DNA-damaging agents involves the activation of mitochondrial apoptotic pathway. Aven has been identified as an antiapoptotic protein and has been shown to activate ATM in response to DNA damage. In this study, we demonstrated that enforced expression of Aven blocks UV-irradiation-, SN-38- or cisplatin-induced apoptosis upstream of mitochondria by stabilising Bcl-xL protein levels in breast cancer cells. Aven silencing by RNA interference markedly enhanced apoptotic response following treatment with DNA-damaging agents. Aven is complexed with Bcl-xL in untreated breast cancer cells and treatment with DNA-damaging agents led to decreased Aven/Bcl-xL interaction. Importantly, Bcl-xL was necessary for the prosurvival activity of Aven and depletion of Bcl-xL abrogated Aven-mediated protection against DNA damage-induced apoptosis. Analysis of breast cancer tissue microarrays revealed decreased Aven nuclear expression in breast cancer tissues compared with non-neoplastic breast tissues. In particular, we detected reduced nuclear expression of Aven in infiltrating ductal carcinoma and papillary carcinoma breast cancer subtypes compared with non-neoplastic breast tissues and infiltrating lobular breast cancer tissues. Our results suggest that Aven is an important mediator in DNA damage-induced apoptotic signalling in breast cancer cells and its nuclear expression is altered in breast cancer tissues, which may contribute to genomic instability in breast cancer tumours.en_US
dc.description.sponsorshipSabancı Üniversitesitr_TR
dc.identifier.citationKütük, Ö. vd. (2010). "Aven blocks DNA damage-induced apoptosis by stabilising Bcl-xL". European Journal of Cancer, 46(13), 2494-2505.en_US
dc.identifier.endpage2505tr_TR
dc.identifier.issn0959-8049
dc.identifier.issn1879-0852
dc.identifier.issue13tr_TR
dc.identifier.pubmed20619636tr_TR
dc.identifier.scopus2-s2.0-77955922449tr_TR
dc.identifier.startpage2494tr_TR
dc.identifier.urihttps://doi.org/10.1016/j.ejca.2010.06.011
dc.identifier.urihttps://www.sciencedirect.com/science/article/pii/S0959804910004867
dc.identifier.urihttp://hdl.handle.net/11452/23070
dc.identifier.volume46tr_TR
dc.identifier.wos000281994100023tr_TR
dc.indexed.pubmedPubmeden_US
dc.indexed.scopusScopusen_US
dc.indexed.wosSCIEen_US
dc.language.isoenen_US
dc.publisherElsevieren_US
dc.relation.collaborationYurt içitr_TR
dc.relation.journalEuropean Journal of Canceren_US
dc.relation.publicationcategoryMakale - Uluslararası Hakemli Dergitr_TR
dc.rightsinfo:eu-repo/semantics/closedAccessen_US
dc.subjectAvenen_US
dc.subjectBcl-xLen_US
dc.subjectApoptosisen_US
dc.subjectBreast canceren_US
dc.subjectDNA damageen_US
dc.subjectCell-deathen_US
dc.subjectDependent activationen_US
dc.subjectDown-regulationen_US
dc.subjectPoor-prognosisen_US
dc.subjectATMen_US
dc.subjectResistanceen_US
dc.subjectCisplatinen_US
dc.subjectBAKen_US
dc.subjectProteinen_US
dc.subjectOncologyen_US
dc.subject.emtree7 ethyl 10 hydroxycamptothecinen_US
dc.subject.emtree[5 (2,4 dichlorobenzoyl) 2 hydroxyphenyl] acetic aciden_US
dc.subject.emtreeApoptosis inhibitoren_US
dc.subject.emtreeApoptosis regulatory proteinen_US
dc.subject.emtreeCisplatinen_US
dc.subject.emtreeNuclear proteinen_US
dc.subject.emtreeProtein avenen_US
dc.subject.emtreeProtein bcl xlen_US
dc.subject.emtreePsg5 hemagglutinin aven vectoren_US
dc.subject.emtreeUnclassified drugen_US
dc.subject.emtreeApoptosisen_US
dc.subject.emtreeArticleen_US
dc.subject.emtreeBreast canceren_US
dc.subject.emtreeCancer cellen_US
dc.subject.emtreeControlled studyen_US
dc.subject.emtreeDNA damageen_US
dc.subject.emtreeEnzyme activationen_US
dc.subject.emtreeExpression vectoren_US
dc.subject.emtreeHumanen_US
dc.subject.emtreeHuman tissueen_US
dc.subject.emtreeImmunohistochemistryen_US
dc.subject.emtreeIntraductal carcinomaen_US
dc.subject.emtreePapillary carcinomaen_US
dc.subject.emtreePriority journalen_US
dc.subject.emtreeProtein expressionen_US
dc.subject.emtreeProtein stabilityen_US
dc.subject.emtreeRNA interferenceen_US
dc.subject.emtreeTissue microarrayen_US
dc.subject.emtreeUltraviolet irradiationen_US
dc.subject.meshAdaptor proteinsen_US
dc.subject.meshSignal transducingen_US
dc.subject.meshAnimalsen_US
dc.subject.meshApoptosisen_US
dc.subject.meshApoptosis regulatory proteinsen_US
dc.subject.meshBcl-X proteinen_US
dc.subject.meshBreast neoplasmsen_US
dc.subject.meshCell line, tumoren_US
dc.subject.meshDNA damageen_US
dc.subject.meshEnzyme-linked immunosorbent assayen_US
dc.subject.meshFemaleen_US
dc.subject.meshHumansen_US
dc.subject.meshMembrane proteinsen_US
dc.subject.meshMiceen_US
dc.subject.meshMicroarray analysisen_US
dc.subject.meshMitochondriaen_US
dc.subject.meshProto-oncogene proteins C-BCL-2en_US
dc.subject.meshRNA, small interferingen_US
dc.subject.scopusApoptosomes; Apoptotic Protease Activating Factor 1; Caspase 9en_US
dc.subject.wosOncologyen_US
dc.titleAven blocks DNA damage-induced apoptosis by stabilising Bcl-xLen_US
dc.typeArticle
dc.wos.quartileQ1en_US

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