Please use this identifier to cite or link to this item: https://hdl.handle.net/11147/4904
Title: Imatinib-induced apoptosis: A possible link to topoisomerase enzyme inhibition
Authors: Baran, Yusuf
Zencir, Sevil
Çakır, Zeynep
Öztürk, Esra
Topçu, Zeki
Baran, Yusuf
Çakır, Zeynep
Izmir Institute of Technology. Molecular Biology and Genetics
Keywords: BCR/ABL
Apoptosis
Topoisomerase
Chronic myeloid leukaemia
Imatinib
Issue Date: 6-Dec-2011
Publisher: John Wiley and Sons Inc.
Source: Baran, Y., Zencir, S., Çakır, Z., Öztürk, E., and Topçu, Z. (2011). Imatinib-induced apoptosis: A possible link to topoisomerase enzyme inhibition. Journal of Clinical Pharmacy and Therapeutics, 36(6), 673-679. doi:10.1111/j.1365-2710.2010.01224.x
Abstract: Summary What 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.
URI: http://doi.org/10.1111/j.1365-2710.2010.01224.x
http://hdl.handle.net/11147/4904
ISSN: 0269-4727
0269-4727
Appears in Collections:Molecular Biology and Genetics / Moleküler Biyoloji ve Genetik
Scopus İndeksli Yayınlar Koleksiyonu / Scopus Indexed Publications Collection
WoS İndeksli Yayınlar Koleksiyonu / WoS Indexed Publications Collection

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