Emerging Anticancer Potentials of Goniothalamin and Its Molecular Mechanisms

Figure 2

Schematic representation of mechanism of action of goniothalamin (GTN) in cancer cells. GTN mostly induces apoptosis either by DNA damage from oxidative stress where GTN decreases GSH level and increases ROS production or direct effect on DNA. Alternatively, GTN may directly affect mitochondria leading to ROS production. The GTN induced cellular stress response leads to the upregulation of p53 as an initial signal for apoptosis. Once activated, the p53 protein can directly or via processing caspase-2 trigger the release of cytochrome c without loss of membrane potential. This is followed by caspase-9 and caspase-3 subsequently. GTN may also act directly on mitochondria or induce the upregulation of Fas/FasL but that needs to be further investigated.