Unravelling the Nexus: Mitochondrial Oxidative Stress, Tumour Microenvironment, and Escape from Immune Surveillance

The reactive oxygen species (ROS) when formed in excessive amounts in the cell due to mitochondrial respiration the body’s defensive antioxidant system cannot function properly. Sometimes, the impaired antioxidant system fails to deactivate the ROS which further causes unfavourable conditions to the cell and its environment. The affected cellular biomolecules disturb the mitochondrial function which is one of the major causes of cellular death. The huge amount of ROS production is a mediator for tumour growth. When activated by oxidative stress, the processes for tumourigenesis become favourable for cancer growth. Similarly, the cellular components of the tumour microenvironment like immune cells, blood vessels, and extracellular matrix are activated by oxidative stress and eventually, get altered in the presence of ROS. Immune surveillance plays a major role in the detection of abnormal cellular growth. T cells and the natural killer cells (NK cells) are activated by the ROS in the tumour microenvironment. These two cells play a major role in eliminating the transformed cells. But, T cells and NK cells produce excessive amounts of ROS which if not controlled then it becomes detrimental to the healthy cells. The present chapter will highlight the oxidative stress due to the activation of mitochondria and its subsequent role in the tumour microenvironment and the effect on immune surveillance.