Fig. 1

Oxidative stress and redox pathway in normal (above) and cancer cells (below). ROS regulate several signaling events by regulating the transcriptions of different genes in a hypoxic microenvironment that regulate the cell cycle, proliferation, and apoptosis. ROS endorse lipid peroxidation, promote electron leakage, and trigger Ca²⁺ release from intracellular stores. ROS in moderate concentrations activate oncogenes and suppress tumor suppressor genes that in turn increase ROS concentration. Intracellular free Ca²⁺ triggers PKC activation that promotes proliferation. OS also endorses antioxidant genes, promotes angiogenesis, and triggers DNA mutation. In addition, ROS induce HDACs that activate oncogenes and inhibit tumor suppressor genes through epigenetic regulation. Red arrows indicate downstream events and red lines indicate inhibition. Akt, protein kinase B; HDACs, histone deacetylases; HIF-1α, hypoxia-inducible factor 1-alpha; IҡBα, nuclear factor of kappa light polypeptide gene enhancer in B-cells inhibitor, alpha; MAPKs, mitogen-activated protein kinases; NF-κB, nuclear factor kappa-light-chain-enhancer of activated B cells; Nrf-2, nuclear factor erythroid 2-related factor 2; OXO, oxalate oxidase; PI3K, phosphoinositide 3-kinases; PKC, protein kinase C; PTEN, phosphatase and tensin homolog; ROS, reactive oxygen species; TS genes, tumor suppressor genes