Figure 7.

Illustration representing the mechanism of goniothalamin (GTN)-induced human breast-derived MDA-MB-231 cancer cell apoptosis. GTN induced apoptosis by DNA damage from oxidative stress and an increase of ROS production. GTN directly induced mitochondria-mediated stress leading to ROS production, mitochondrial intermembranous protein release and activation with sequential caspases. GTN induced a cellular stress response, which led to the upregulation of pro-apoptotic molecules. GTN also induced ER-stress and an increase in the levels of the ER-stress proteins leading to apoptosis.