Fig. 5

Schematic diagram illustrating the mechanism by which CPS1 promotes the progression of lung adenocarcinoma by inhibiting the ammonia-induced ROS/AMPK/P53/LKB1 signaling pathway. After CPS1 knockdown, the intracellular ammonia metabolism becomes unbalanced, resulting in a significant increase in ammonia levels. The accumulated ammonia induces oxidative stress and generates excessive reactive oxygen species (ROS). Excessive ROS are activated through oxidative modification and phosphorylate AMPK, increasing its phosphorylation level. Phosphorylated AMPK further activates P53 and promotes its formation with LKB1 into a complex, enhancing the activity of LKB1. The activated P53 and LKB1 complex upregulates the expression of pro-apoptotic proteins (such as Bax, Caspase-8, and Caspase-12), thereby inhibiting the proliferation of tumor cells and promoting their apoptosis.