Research Paper Volume 14, Issue 9 pp 3956—3972

Figure 5. Schematic diagram of function regulation mode of ferroptosis genes in SCC. Under the stress of UV, virus or radioactive factors, normal cells lose the control of tumor suppressor gene TP53 and proliferate malignantly. At the same time, excessive activation of ROS function in the intracellular environment causes stress damage to mitochondria and endoplasmic reticulum. The imbalance of NQO1 homeostasis in SCC tumor cells cannot guarantee the stabilization of P53 and the inhibitory effect of ROS. Moreover, under immune surveillance, the cytolytic activity of local immune cells is enhanced, and endocytosis is formed through antigen-antibody binding, which further induces cancer cells undergo apoptosis or necrosis. However, in the early stage, under the regulation of NQO1 homeostasis, some cancer cells adapt to the higher ROS environment. These “super tumor cells” accelerate the progression of SCC and increase the degree of malignancy. Ferroptosis is a process of cell necrosis catalyzed by iron. When a large amount of Fe2+ accumulates in the intracellular environment, it will synergistically increase the function of ROS. The overactivation of HMOX1 and STEAP3 increase Fe2+ levels through Heme and iron pool, respectively.