Figure 8.

Schematic representation proposed for the plausible mechanisms of action of 10058-F4 in APL-derived NB4 cells. Through inhibition of c-Myc, 10058-F4 augmented the intracellular level of ROS and induced caspase-3-dependent apoptotic cell death in NB4 cells through suppression of the NF-κB signaling pathway. This favorable anti-leukemic activity could be attenuated through activation of the PI3K signaling pathway. Suppression of the PI3K axis using CAL-101 eliminated the compensatory effect of this pathway on 10058-F4-induced cytotoxic effect and promoted a more significant apoptotic cell death in NB4 cells