of 10 μM for 72 h. The 4-IPMCP treatment induced apoptosis in K562 cells by down-regulating Bcl-2, overexpressing Bax, and increasing the Bax/Bcl-2 ratio. This treatment also stimulated cellular ROS generation and induced cell cycle arrest in the sub-G1 phase. This study demonstrated the effects of 4-IPMCP on cell cycle arrest, anticancer properties, and oxidative stress-induced apoptosis in chronic myeloid leukemia (CML) K562 cells. Since this agent has the potential to inactivate cancer cells and treat patients, it can be considered a viable candidate for further drug studies in cancer treatment.
Barzegari et al. (Thu,) studied this question.