Mechanistic study of glutamine metabolic reprogramming driving non-small cell lung cancer progression via the FGF17-FGFR4 axis mediating epithelial-mesenchymal transition

As a critical driver of glutamine metabolic reprogramming, FGF17-activated under conditions of GLUL overexpression-stimulates the FGFR4/MEK5/ERK5/NRF2 signaling cascade to maintain redox homeostasis and promote invasion, thereby accelerating NSCLC progression. Targeted intervention of the pathway reverses malignant phenotypes and enhances chemosensitivity. These findings highlight FGF17 as a potential therapeutic target for NSCLC and provide new insights into tumor metabolism and EMT, thereby may paving the way for novel combination therapies.