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

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‑

SUBMITTER: Liu YH 

PROVIDER: S-EPMC8144938 | biostudies-literature | 2021 Jul

REPOSITORIES: biostudies-literature