Imatinib-induced apoptosis: a possible link to topoisomerase enzyme inhibition

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dc.contributor.authorBaran, Y.
dc.contributor.authorZencir, S.
dc.contributor.authorCakir, Z.
dc.contributor.authorOzturk, E.
dc.contributor.authorTopcu, Z.
dc.date.accessioned2019-10-27T21:35:20Z
dc.date.available2019-10-27T21:35:20Z
dc.date.issued2011
dc.departmentEge Üniversitesien_US
dc.description.abstractWhat is known and Objective: Imatinib is a specific BCR/ABL inhibitor, commonly used for the treatment of chronic myeloid leukaemia (CML), a hematological malignancy resulting from a chromosomal translocation that generates the BCR/ABL fusion protein. Recent studies showed that the imatinib has cytotoxic and apoptotic effects on many BCR/ABL-negative cancers. Numerous compounds with cytotoxic potential exert their functions by interfering with the DNA topoisomerase. In this study, we examined the effects of imatinib on tumour cell-killing in relation to DNA topoisomerase enzyme inhibition. Methods: We determined the cytotoxicity by cell proliferation assay (XTT; tetrazolium hydroxide), using the human K562 CML cells, and loss of mitochondrial membrane potential by monitoring the changes in caspase-3 enzyme activity. Type I and II topoisomerase activities were measured by supercoiled plasmid relaxation and minicircle DNA decatenation assays respectively. Results and Discussion: Imatinib-induced apoptosis and inhibited cell proliferation in a dose-dependent manner. We also found that the imatinib was effective in both type I and type II topoisomerase reactions to a varying degree between 94% and 7% for the concentration range of 1 mM-0.02 mm in a dose-dependent manner. What is new and Conclusion: Our results suggest that the inhibition of topoisomerases may be a significant factor in imatinib-induced apoptosis in CML.en_US
dc.description.sponsorshipScientific and Technological Research Council of TurkeyTurkiye Bilimsel ve Teknolojik Arastirma Kurumu (TUBITAK) [TBAG108T548]en_US
dc.description.sponsorshipThis study was partially supported by the grant from The Scientific and Technological Research Council of Turkey (Grant No: TBAG108T548) (Z.T.). We would like thank to Izmir Institute of Technology, Biotechnology and Bioengineering Research Facility staff for their technical help.en_US
dc.identifier.doi10.1111/j.1365-2710.2010.01224.xen_US
dc.identifier.endpage679en_US
dc.identifier.issn0269-4727
dc.identifier.issue6en_US
dc.identifier.pmid21105880en_US
dc.identifier.scopusqualityN/Aen_US
dc.identifier.startpage673en_US
dc.identifier.urihttps://doi.org/10.1111/j.1365-2710.2010.01224.x
dc.identifier.urihttps://hdl.handle.net/11454/45836
dc.identifier.volume36en_US
dc.identifier.wosWOS:000297023500005en_US
dc.identifier.wosqualityQ3en_US
dc.indekslendigikaynakWeb of Scienceen_US
dc.indekslendigikaynakScopusen_US
dc.indekslendigikaynakPubMeden_US
dc.language.isoenen_US
dc.publisherWiley-Blackwellen_US
dc.relation.ispartofJournal of Clinical Pharmacy and Therapeuticsen_US
dc.relation.publicationcategoryMakale - Uluslararası Hakemli Dergi - Kurum Öğretim Elemanıen_US
dc.rightsinfo:eu-repo/semantics/closedAccessen_US
dc.subjectapoptosisen_US
dc.subjectBCR/ABLen_US
dc.subjectchronic myeloid leukaemiaen_US
dc.subjectimatiniben_US
dc.subjecttopoisomeraseen_US
dc.titleImatinib-induced apoptosis: a possible link to topoisomerase enzyme inhibitionen_US
dc.typeArticleen_US

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