Molecular Biology and Genetics / Moleküler Biyoloji ve Genetik

Permanent URI for this collectionhttps://hdl.handle.net/11147/9

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Author: search.filters.author.Çakır, ZeynepWoS Q: search.filters.wosQuartile.Q3

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  • Article
    Citation - WoS: 5
    Citation - Scopus: 7
    Imatinib-Induced Apoptosis: a Possible Link To Topoisomerase Enzyme Inhibition
    (John Wiley and Sons Inc., 2011) Baran, Yusuf; Zencir, Sevil; Çakır, Zeynep; Öztürk, Esra; Topçu, Zeki
    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.
  • Article
    Citation - WoS: 18
    Citation - Scopus: 16
    Suppression of Stat5a Increases Chemotherapeutic Sensitivity in Imatinib-Resistant and Imatinib-Sensitive K562 Cells
    (Informa Healthcare, 2010) Kosova, Buket; Tezcanlı, Burçin; Ekiz, Hüseyin Atakan; Çakır, Zeynep; Selvi, Nur; Dalmızrak, Ayşegül; Yandım, Melis Kartal; Gündüz, Ufuk; Baran, Yusuf
    STAT proteins are cytoplasmic transcription factors that are involved in the regulation of numerous cellular activities such as cell growth, differentiation, and survival. In this study, we aimed to identify the expression pattern of STAT genes in imatinib-sensitive and-resistant K562 cells, and further, to reveal the effects of STAT5A siRNA knockdown on cell growth and apoptosis induction. The XTT cell proliferation assay showed that both sensitive and resistant K562 cells were sensitized to imatinib upon transfection with STAT5A siRNA. Caspase-3 enzyme activity was increased significantly in both cells. These results may open up new opportunities to overcome chemotherapeutic resistance in leukemia. © 2010 Informa UK, Ltd.