[Corrigendum] ND­09 inhibits chronic myeloid leukemia K562 cell growth by regulating BCR­ABL signaling.

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].

ND­09 inhibits chronic myeloid leukemia K562 cell growth by regulating BCR­ABL signaling.

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.