Figure 10

Schematic model of cell death mechanism in CACF-induced responses in melanoma A375 cells. CACF induces intracellular ROS production due to elevated oxidative stress. This initiates various intracellular changes including increased membrane permeability and reduced MMP which subsequently causes cytochrome c release from the mitochondria. Cytoplasmic cytochrome c activates caspase pathway molecules, including caspase-9 and caspase-3/7. Activation of caspase molecules subsequently leads to nuclear fragmentation. CACF treatment also triggers p53 expression that may initiate apoptosis activity through reduction of anti-apoptotic Bcl-2 level. On the other hand, CACF prevented NF-κB nuclear translocation, which could induce Bcl-2 transactivation and maintain cell survival in A375 melanoma cells.