Figure 4.

A schematic representation of the mechanisms and role of autophagy modulation in the anticancer action of GNM. GNM induce autophagy through oxidative/ER stress and AMPK/AKT/mTORC1, MAPK, or TLR signaling, but can simultaneously block autophagic flux by causing lysosomal dysfunction. This leads to accumulation of autophagic mediators such as LC3, p62, and ATG5, which participate in apoptotic, necrotic, or necroptotic death of tumor cells. GNM-induced autophagy could also modulate anti-tumor immune responses. AMPK, AMP-activated protein kinase; ATG, autophagy-related; ER, endoplasmic reticulum; GNM, graphene nanomaterials; LC3, microtubule-associated light chain 3; MAPK, mitogen-activated protein kinases; mTOR, mechanistic target of rapamycin complex 1; ROS, reactive oxygen species; TLR, Toll-like receptors.