FIGURE 3.

A schematic representation of the dual role of reactive oxygen species (ROS) in cancer. Oxidative stress in a tumour microenvironment promotes superoxide dismutase (SOD) catalysed break down of superoxides into hydrogen peroxide, which in presence of excess free undergoes Fenton reaction leading to an overaccumulation of free radicals/ROS, responsible for lipid peroxidation and loss of cell membrane integrity, a common event favouring both pro‐tumorigenesis and anti‐tumorigenesis, the fate being majorly dependent on comparative ROS levels against cellular antioxidant defence (AOD). While iron‐generated free radicals may stimulate anti‐tumorigenic signalling through ferroptosis induction and drive oxidative stress‐promoted tumour clearance, cancer cells possess the ability to adapt to the hypoxic environment, triggering cellular transformation pathways through irreversible cell membrane damage, therefore, facilitating their survival and proliferation.