Figure 3.

Mechanisms of ROS-mediated cancer cell death. Elevated levels of ROS can orchestrate cancer cell death by apoptosis, necrosis, and autophagy. ROS-mediated activation of Bax, death receptors (DR), and caspases elicits apoptotic cell death. Increased oxidative stress can also lead to necrosis by forming receptor interacting protein kinase, RIPK-1/RIPK-3 complex. Moreover, NOX can interact with TNF to facilitate necrosis. Redox stress-induced inhibition of mammalian target of rapamycin (mTOR) activity and activation of AMP-activated protein kinase (AMPK) stimulate vacuolar protein sorting 34 (VPS 34) complex that results in the commencement of autophagy.