Inhibition of c-Myc by 10058-F4 overcomes imatinib resistance in chronic myeloid leukemia cells |
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Authors: | LONG Zi-jie FANG Zhi-gang PAN Xiao-na FAN Rui-fang LIN Dong-jun |
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Affiliation: | Department of Hematology, The Third Affiliated Hospital of Sun Yat-sen University, Sun Yat-sen Institute of Hematology, Sun Yat-sen University, Guangzhou 510630, China. |
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Abstract: | AIM:To investigate the effect of c-Myc inhibitor 10058-F4 on human chronic myeloid leukemia (CML) K562 cells and imatinib-resistant K562/G cells. METHODS:The protein expression of c-Myc was detected by Western blotting. Cell proliferation was evaluated by MTT assay and colony formation assay. PI staining was used to determine the cell cycle distribution. Annexin V-PI staining was applied for apoptosis detection. RESULTS:Imatinib-resistant K562/G cells displayed lower sensitivity to imatinib than K562 cells with high expression of c-Myc. Treatment with specific c-Myc inhibitor 10058-F4 inhibited the cell proliferation in a dose- and time-dependent manner, and K562/G displayed more sensitivity to 10058-F4 than K562 cells. 10058-F4 also induced cell cycle arrest in G0/G1 phase and induced apoptotic cell death in the 2 cells. Importantly, 10058-F4 suppressed the colony formation ability in K562 and K562/G cells. CONCLUSION:c-Myc is a novel target to overcome imatinib-induced drug resistance, and c-Myc inhibitor provides a new approach in CML therapy. |
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Keywords: | c-Myc 10058-F4 Imatinib resistance Chronic myeloid leukemia |
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