ROS and oncogenesis with special reference to EMT and stemness

Abstract

Elevation of the level of intracellular reactive oxygen species (ROS) has immense implication in the biological system. On the one hand, ROS promote the signaling cascades for the maintenance of normal physiological functions, the phenomenon referred to as redox biology, and on the other hand increased ROS can cause damages to the cellular macromolecules as well as genetic material, the process known as oxidative stress. Oxidative stress acts as an etiological factor for wide varieties of pathologies, cancer being one of them. ROS is regarded as a "double-edged sword" with respect to oncogenesis. It can suppress as well as promote the malignant progression depending on the type of signaling pathway it uses. Moreover, the attribution of ROS in promoting phenotypic plasticity as well as acquisition of stemness during neoplasia has become a wide area of research. The current review discussed all the aspects of ROS in the perspective of tumor biology with special reference to epithelial-mesenchymal transition (EMT) and cancer stem cells.

Keywords: Cancer; Cancer stem cells; EMT; Hypoxia; Oxidative stress; ROS.