Abstract
Aims: Chronic myeloid leukemia (CML) is a type of leukemia characterized by the Philadelphia (Ph) chromosome encoding the BCR-ABL protein. Significant success has been achieved in the treatment of CML with the development of agents that target this protein and inhibit its activity, but the resistance that develops in patients against these drugs limits absolute success. One of the main reasons for the resistance problem is the ineffectiveness of current therapies for CML stem cells. Apigenin (4',5,7- trihydroxyflavone) is a flavanoid found in various vegetables and fruits and has the effects of suppressing proliferation and inducing apoptosis in different cancer types. In this study, we aimed to determine the therapeutic potential of apigenin on K562 CML stem cells. Methods: The effects of apigenin on the proliferation of K562 CML stem cells were determined by an XTT cell proliferation assay. Apoptotic effects of apigenin on K562 CML stem cells were determined by changes in mitochondrial membrane potential (MZP), caspase-3 enzyme activity, and the Annexin-V method using flow cytometry. Results: The proliferation of K562 CML stem cells exposed to increasing doses of Apigenin (1-40 nM) for 48 hours decreased dose-dependently, and the IC50 value of Apigenin was calculated at 3 nM. Compared to the control group, an increase in caspase-3 enzyme activity was calculated in stem cells treated with apigenin at the same doses. Disruptions in the mitochondrial membrane potential of Apigenin-treated CML stem cells and Annexin-V assay results also showed that Apigenin dose-dependently induced apoptosis and caused significant increases in the apoptotic cell population. Conclusion: It was shown for the first time in this study that apigenin may have therapeutic effects on CML stem cells. It was determined that this effect of apigenin was achieved by triggering caspase-3 enzyme activity and disruptions in the mitochondrial membrane.
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