ROS-Mediated Therapeutic Strategy in Chemo-/Radiotherapy of Head and Neck Cancer

Figure 4

ROS is implicated in the modulation in the chemo-/radiotherapy of HNC. ROS can directly and indirectly affect the efficiency of chemotherapy drugs such as cisplatin and 5-Fu and/or radiation therapy in HNC. A direct effect is seen in terms of ROS-induced lethal genetic damage. Indirect mechanisms include cell death regulation such as apoptosis and autophagy, DNA damage repair, drug metabolism, cancer stem cell (CSC) characteristics, and tumor microenvironment (TME) which are modulated by ROS in the chemotherapy of HNC. Radiotherapy exerts its function through induction of DNA damage within the cell. Except for drug metabolism, other mechanisms are all involved in ROS-mediated radiotherapy efficacy in HNC. Because of the dual role of ROS, the complex modulation network can adapt towards the killing effect of cancer cells or readapting the therapy stimuli. Generally, low and chronic ROS may call for more antioxidant stress defense to protect cancer cells, while high and acute ROS may kill cancer cells with no margin for adaptation. Note. ROS: reactive oxygen species; HNC: head and neck cancer; 5-Fu: 5-flurouracil; DNA: deoxyribonucleic acid; CSC: cancer stem cell; TME: tumor microenvironment.