Reactive Oxygen Species (ROS) in Cancer: Review Article
Gehan Abdel Naser Abdel Rahman
Department of Oral and Maxillofacial Pathology department, Faculty of Oral and Dental Medicine, South Valley University & Department of Oral Pathology, Faculty of Dentistry, Minia University, Egypt
Dr. Gehan Abdel Naser Abdel Rahman, Department of Oral and Maxillofacial Pathology department, Faculty of Oral and Dental Medicine, South Valley University & Department of Oral Pathology, Faculty of Dentistry, Minia Universit
Keywords: ROS; Antioxidant; Cancer Cells; Oxidative Stress
Background Cancer is one of the major heterogeneous disease with high morbidity and mortality with poor prognosis. Elevated levels of reactive oxygen species (ROS), alteration in redox balance, and deregulated redox signaling are common hallmarks of cancer progression and resistance to treatment. Mitochondria contribute mainly in the generation of ROS during oxidative phosphorylation. Elevated levels of ROS have been detected in cancers cells due to high metabolic activity, cellular signaling, peroxisomal activity, mitochondrial dysfunction, activation of oncogene, and increased enzymatic activity of oxidases, cyclooxygenases, lipoxygenases, and thymidine phosphorylases. ROS, now appreciated for their cellular signaling capabilities, have a dual role in cancer. On the one hand, ROS can promote protumorigenic signaling, facilitating cancer cell proliferation, survival, and adaptation to hypoxia. On the other hand, ROS can promote antitumorigenic signaling and trigger oxidative stress–induced cancer cell death. To hyperactivate the cell signaling pathways necessary for cellular transformation and tumorigenesis, cancer cells increase their rate of ROS production compared with normal cells. Concomitantly, in order to maintain ROS homeostasis and evade cell death, cancer cells increase their antioxidant capacity. Compared with normal cells, this altered redox environment of cancer cells may increase their susceptibility to ROSmanipulation therapies. In this article, we discuss the role of ROS in cancer, the mechanisms underlying ROS signaling, and the opposing cancer therapeutic approaches to targeting ROS.
This is an open access article distributed under the Creative Commons Attribution License which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. (CC BY 4.0).