Oxidative Stress Player in Head and Neck Cancer Therapy Response

Oxidative stress results from the imbalance between two opposite processes, the generation and removal of reactive oxygen species (ROS). In normal cells, ROS are present in low concentrations and stimulate intracellular signaling pathways leading to the activation of key transcription factors. In contrast, tumor cells have a more intense metabolism and require higher amounts of generated ROS to maintain their high proliferation rate. In tumor pathogenesis, there are a plethora of factors involved in the oxidative stress network. Lowering the ROS generation below a certain threshold promotes the production of antioxidants inducing apoptosis resistance of tumor cells. Based on its cell concentrations, high or low, ROS’s role can be beneficial or detrimental to the body’s health. The benefic role in the regulation of metabolic and intracellular signaling pathways leads to the proper development and proliferation of cells. The detrimental role is responsible for the cellular and tissue damages by faulty antioxidant and/or DNA repair mechanisms. Many therapeutical anticancer agents are used to increase ROS’s cellular level to overcome the activity of scavenging/antioxidant enzymes of the tumor cell and hence induce apoptosis. Moreover, Ros can induce the activation of survival signaling pathways and inactivation of death signaling events, accompanied by the induction of “multidrug resistance” properties in the tumor cell, hindering therefore the overall efficacy of cancer treatment. This paper is focused on the multiplayer role of oxidative stress in fundamental processes appending to cancer pathogenesis. Also, we will discuss oxidative stress as a modulator of therapy response to combat drug resistance.