RESUMO
Subsequently to the publication of this paper, the authors have realized that an error was made during the compilation of Fig. 2A as it appeared on p. 4. Essentially, the partial Q23 images of the '1.56 µm' group were inadvertently copied across to the Q23 images of the '3.12 µm' group, leading to the cell number of the Q23 quadrant being the same for both the 1.56 µm and the 3.12 µm groups, and also leading the total cell number of the 3.12 µm group being calculated as 106.97%, which was clearly incorrect (the total percentage should have added up to 100%). The corrected version of Fig. 2, showing the correct data for the Q23 images in the '3.12 µm' group, is shown on the next page. Note that this error did not significantly affect the results or the conclusions reported in this paper, and all the authors agree with the publication of this Corrigendum. The authors are grateful to the Editor of Oncology Reports for allowing them this opportunity to publish a corrigendum, and apologize to the readership for any inconvenience caused. [Oncology Reports 46: 136, 2021; DOI: 10.3892/or.2021.8087].
RESUMO
Chronic myeloid leukemia (CML) accounts for approximately 15% of new adult leukemia cases. The fusion gene BCRABL is an important biological basis and target for CML. In the present study, a novel compound, ND09, was developed and its inhibitory effect and mechanism of action on CML growth were evaluated using RTPCR and western blot analysis. The results showed that ND09 demonstrated a high level of inhibitory action toward CML cells overexpressing BCRABL and induced K562 cell apoptosis through the mitochondrial pathway. Notably, combined ND09 and BCRABL siRNA treatment could better inhibit cell proliferation and induce apoptosis in K562 cells. Furthermore, this growth effect of BCRABL siRNA could be fully rescued by transfection with BCRABL. ND09 exhibited a good fit within BCRABL and occupied its ATPbinding pocket, thus altering BCRABL kinase activity. Therefore, ND09 downregulated the phosphorylation of BCRABL and ABL, ultimately inhibiting the downstream signaling pathways in K562 cells. These findings suggest that ND09 induces growth arrest in CML cells by targeting BCRABL.