ND‑09 inhibits chronic myeloid leukemia K562 cell growth by regulating BCR‑ABL signaling Corrigendum in /10.3892/or.2023.8518

Liu,Yan-Hong; Zhu,Man; Lei,Pan-Pan; Pan,Xiao-Yan; Ma,Wei-Na

doi:10.3892/or.2021.8087

ND‑09 inhibits chronic myeloid leukemia K562 cell growth by regulating BCR‑ABL signaling

Corrigendum in: /10.3892/or.2023.8518

Authors:
- Yan-Hong Liu
- Man Zhu
- Pan-Pan Lei
- Xiao-Yan Pan
- Wei-Na Ma
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Affiliations: School of Pharmacy, Health Science Center, Xi'an Jiaotong University, Xi'an, Shaanxi 710061, P.R. China
Published online on: May 20, 2021 https://doi.org/10.3892/or.2021.8087
Article Number: 136
Copyright: © Liu et al. This is an open access article distributed under the terms of Creative Commons Attribution License.

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Abstract

Chronic myeloid leukemia (CML) accounts for approximately 15% of new adult leukemia cases. The fusion gene BCR‑ABL is an important biological basis and target for CML. In the present study, a novel compound, ND‑09, was developed and its inhibitory effect and mechanism of action on CML growth were evaluated using RT‑PCR and western blot analysis. The results showed that ND‑09 demonstrated a high level of inhibitory action toward CML cells overexpressing BCR‑ABL and induced K562 cell apoptosis through the mitochondrial pathway. Notably, combined ND‑09 and BCR‑ABL siRNA treatment could better inhibit cell proliferation and induce apoptosis in K562 cells. Furthermore, this growth effect of BCR‑ABL siRNA could be fully rescued by transfection with BCR‑ABL. ND‑09 exhibited a good fit within BCR‑ABL and occupied its ATP‑binding pocket, thus altering BCR‑ABL kinase activity. Therefore, ND‑09 downregulated the phosphorylation of BCR‑ABL and ABL, ultimately inhibiting the downstream signaling pathways in K562 cells. These findings suggest that ND‑09 induces growth arrest in CML cells by targeting BCR‑ABL.

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