Abstract

In a normal physiological state, Nrf2-Keap1 pathway is associated with antioxidation progress. Mostly, Nrf2 interacts with Keap1 and shows a low cellular abundance. When the intracellular oxidative stress level increases, Nrf2 uncouples with Keap1 then performs nuclear translocation to regulate the RNA levels of its downstream targets, control the redox-related balance in the cell and exert cytoprotective effect. The mutation of related factors in the signal pathway will lead to the abnormality of oxidative damage, which may lead to lung cancer. Therefore, the remission treatment of lung cancer can be achieved through the inhibition of Nrf2-Keap1pathway. We will concentrate on Nrf2 and Keap1's structural and functional domains in the review. Then we summary the mutation sites and signal pathway of Nrf2-Keap1. Most importantly, we discuss the potential clinical application of Nrf2-Keap1 and further adopt the method of molecular docking to screen the small molecules acting on Nrf2-Keap1 to provide the potential improvement to current lung cancer treatment.

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