Fig. 1
Neddylation inhibitor blunted the therapeutic function of BCR::ABL1-targeting TKIs. (A, B) K562 cells were treated with imatinib (0.5 µM), nilotinib (0.1 µM), ponatinib (2.5 nM) (A), or asciminib (50 nM) (B) in the presence or absence of MLN4924 (25 µM) for 24 h. Cell viability was evaluated by CCK8. (C) KU812 cells were treated with imatinib in the presence or absence of MLN4924 for 24 h. Cell viability was evaluated by CCK8. (D) K562 cells were treated with the indicated TKIs in the presence or absence of MLN4924 (25 µM) for 24 h, cell counting was performed following Hoechst staining. (E) K562 cells were treated with imatinib (0.5 µM) in the presence or absence of MLN4924 (25 µM) for 24 h. Cell apoptosis was evaluated by Annexin V/PI staining. (F) K562 cells were treated with imatinib (0.5 µM), nilotinib (0.1 µM), or ponatinib (2.5 nM) in the presence or absence of TAS4464 (1 µM) for 24 h. Cell viability was evaluated by CCK8. (G) K562 cells were treated with the indicated TKIs in the presence or absence of TAS4464 (1 µM) for 24 h, cell counting was performed following Hoechst staining. (H) UBA3 was silenced in K562 cells, followed by imatinib (0.5 µM) treatment for 24 h, cell viability was evaluated by CCK8. Unpaired, two-tailed Student’s t-test. *p < 0.05; **p < 0.01; ***p < 0.001.
