Fig. 7. Schematic diagram of the function and mechanisms of MBZ in CML cells.
The anticancer effect of MBZ is mediated by at least two processes: one involving downregulated p-BCR/ABL and its downstream signaling pathways, and the other involving disrupted microtubule dynamics. This molecule downregulates p-BCR/ABL, p-STAT5 and MAPK signalling pathway, thereby inhibiting the growth of CML cells. MBZ blocks microtubule polymerization, results in cell cycle arrest at mitosis and triggers mitotic catastrophe event, which induces apoptosis in CML cells. In addition, MBZ triggers substantial DNA damage by delaying repair processing, leading to enhanced genomic instability and mitotic catastrophe. MBZ, mebendazole; CML, chronic myeloid leukemia; ATM, ataxia-telangiectasia mutated; DNA-PKcs, DNA-dependent protein kinase.
© Korean J Physiol Pharmacol
