Abstract
Emerging of reactive oxygen species (ROS) on the earth with the first oxygen molecule in the atmosphere around 2.4–3.8 billion years ago, and they have been associated with aerobic life ever since. Insufficient reduction of oxygen molecule led to the creation of chemically more reactive species such as superoxide anion (O2−), hydrogen peroxide (H2O2), hydroxyl radicals (OH•), and singlet oxygen (1O2), collectively coined as reactive oxygen species (ROS). Both the extrinsic environment and endogenous metabolism contribute to physiologically relevant ROS in human cells. Excessive production of ROS in the cells can structurally and/or functionally degrade the macromolecules such as nucleic acids, proteins, and lipids which has been linked to oxidative stress mediating diseases, those are considered to be oncogenic, promoting genomic instability, and tumorigenesis. There has been a great deal of study relating ROS to many physiological functions related to variety of disorders, include cancer, diabetes, atherosclerosis, and neurodegeneration. Cancer cells augment their rate of ROS production to overactivate tumorigenic signaling events by promoting oncogenic mutations, losing tumor suppressors, enhancing their metabolism, and adjusting to hypoxia. In this chapter, we are going to discuss about the sources of ROS, role in cancer and how the key transcription factors such as NRF2, P53, and HIF-1α can be used as a targeted for cancer therapy.