Please use this identifier to cite or link to this item: http://hdl.handle.net/11452/25386
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dc.contributor.authorYerlikaya, Azmi-
dc.contributor.authorOkur, Emrah-
dc.date.accessioned2022-03-28T11:50:13Z-
dc.date.available2022-03-28T11:50:13Z-
dc.date.issued2012-10-
dc.identifier.citationYerlikaya, A. vd. (2012). "The p53-independent induction of apoptosis in breast cancer cells in response to proteasome inhibitor bortezomib". Tumor Biology, 33(5), 1385-1392.en_US
dc.identifier.issn1010-4283-
dc.identifier.urihttps://doi.org/10.1007/s13277-012-0386-3-
dc.identifier.urihttps://link.springer.com/article/10.1007%2Fs13277-012-0386-3-
dc.identifier.urihttp://hdl.handle.net/11452/25386-
dc.description.abstractAn important hallmark of cancer cells is acquired resistance toward apoptosis. The apoptotic pathway is the most well-defined cell death program and is characterized by several morphological and biochemical features. The tumor suppressor protein p53 is a critical regulator of apoptosis in many cell types. p53 stimulates a wide network of signals that act through either extrinsic or intrinsic pathways of apoptosis. However, a number of studies have shown that apoptosis can be induced in a p53-independent manner as well. In this study, we examined the mechanism of apoptosis in p53-null breast cancer cells in response to the proteasome inhibitor bortezomib. Initially, we determined the p53 status of 4T1 breast carcinoma and 4THMpc (a highly mestatic derivative of 4T1) cells and verified that both cells are p53 deficient. It was subsequently shown that apoptosis can be induced in both cells in a dose-dependent manner in response to bortezomib treatment, based on DNA fragmentation evidence. Western blot analyses of ubiquitin-protein conjugates additionally showed that the proteasome is potently inhibited by bortezomib in p53-null 4T1 and 4THMpc cells. The results presented in the current study also show that caspase-3 is significantly activated in response to the treatment with bortezomib, implying that induction of apoptosis in these p53-deficient cells is occuring via caspase-3. The additional results presented here suggest that the pro-apoptotic proteins Bad, Noxa, and Puma are not critical regulators of apoptosis induction in p53-null 4T1 and 4THMpc cells. Similarly, there was no difference in the expression level of Mcl-1 in treated cells, suggesting that this anti-apoptotic protein is also uninvolved in the apoptotic response resulting from bortezomib treatment. In contrast, a very significant upregulation of the anti-apoptotic protein Hsp25/27 was detected in these p53-deficient cells after treatment with bortezomib. If the increased expression of Hsp25/27 protein levels are muting the apoptotic effects of the bortezomib treatment, then the apoptosis-inducing effects of such proteasome inhibitors might be increased with approaches simultaneously inhibiting Hsp25/27 protein in p53-deficient cells.en_US
dc.language.isoenen_US
dc.publisherSage Publicationsen_US
dc.rightsinfo:eu-repo/semantics/closedAccessen_US
dc.subjectOncologyen_US
dc.subjectApoptosisen_US
dc.subjectBortezomiben_US
dc.subjectCanceren_US
dc.subjectCaspaseen_US
dc.subjectP53en_US
dc.subjectProteasomeen_US
dc.subjectMelanoma-cellsen_US
dc.subjectUp-regulationen_US
dc.subjectLymphoma-cellsen_US
dc.subjectDna-damageen_US
dc.subjectIn-vitroen_US
dc.subjectNoxaen_US
dc.subjectMechanismen_US
dc.subjectDeathen_US
dc.subjectDegradationen_US
dc.subject.meshAntineoplastic agentsen_US
dc.subject.meshApoptosisen_US
dc.subject.meshApoptosis regulatory proteinsen_US
dc.subject.meshBoronic acidsen_US
dc.subject.meshBreast neoplasmsen_US
dc.subject.meshCaspase 3en_US
dc.subject.meshCell line, tumoren_US
dc.subject.meshEnzyme activationen_US
dc.subject.meshFemaleen_US
dc.subject.meshGene expression regulation, neoplasticen_US
dc.subject.meshHumansen_US
dc.subject.meshPyrazinesen_US
dc.subject.meshTumor suppressor protein p53en_US
dc.titleThe p53-independent induction of apoptosis in breast cancer cells in response to proteasome inhibitor bortezomiben_US
dc.typeArticleen_US
dc.identifier.wos000309354600015tr_TR
dc.identifier.scopus2-s2.0-84868091512tr_TR
dc.relation.tubitak109S035tr_TR
dc.relation.publicationcategoryMakale - Uluslararası Hakemli Dergitr_TR
dc.contributor.departmentUludağ Üniversitesi/Tıp Fakültesi/Tıbbi Biyokimya Anabilim Dalı.tr_TR
dc.identifier.startpage1385tr_TR
dc.identifier.endpage1392tr_TR
dc.identifier.volume33tr_TR
dc.identifier.issue5tr_TR
dc.relation.journalTumor Biologyen_US
dc.contributor.buuauthorUlukaya, Engin-
dc.contributor.researcheridK-5792-2018tr_TR
dc.relation.collaborationYurt içitr_TR
dc.identifier.pubmed22477712tr_TR
dc.subject.wosOncologyen_US
dc.indexed.wosSCIEen_US
dc.indexed.scopusScopusen_US
dc.indexed.pubmedPubMeden_US
dc.wos.quartileQ3en_US
dc.contributor.scopusid6602927353tr_TR
dc.subject.scopusProteasome Inhibitors; Carfilzomib; Bortezomiben_US
dc.subject.emtreeBevacizumaben_US
dc.subject.emtreeCaspase 3en_US
dc.subject.emtreeDnaen_US
dc.subject.emtreeHeat shock protein 27en_US
dc.subject.emtreeProteasomeen_US
dc.subject.emtreeProtein baden_US
dc.subject.emtreeProtein mcl 1en_US
dc.subject.emtreeProtein Noxaen_US
dc.subject.emtreeProtein p53en_US
dc.subject.emtreePuma proteinen_US
dc.subject.emtreeUbiquitinen_US
dc.subject.emtreeApoptosisen_US
dc.subject.emtreeArticleen_US
dc.subject.emtreeBreast canceren_US
dc.subject.emtreeBreast carcinomaen_US
dc.subject.emtreeCancer cell cultureen_US
dc.subject.emtreeConcentration responseen_US
dc.subject.emtreeControlled studyen_US
dc.subject.emtreeDna fragmentationen_US
dc.subject.emtreeDrug mechanismen_US
dc.subject.emtreeDrug responseen_US
dc.subject.emtreeEnzyme activationen_US
dc.subject.emtreeNull cellen_US
dc.subject.emtreePriority journalen_US
dc.subject.emtreeProtein analysisen_US
dc.subject.emtreeProtein deficiencyen_US
dc.subject.emtreeProtein expressionen_US
dc.subject.emtreeSignal transductionen_US
dc.subject.emtreeUpregulationen_US
dc.subject.emtreeWestern blottingen_US
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