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Article highlights NSCLC tumors exhibit metabolic heterogeneity with subpopulations relying on glycolysis, OXPHOS, or mixed phenotypes depending on environmental context Metabolic plasticity enables cancer cells to switch between energy pathways, contributing to therapeutic resistance Key oncogenic drivers (KRAS, EGFR, LKB1, KEAP1) distinctly reprogram metabolism through effects on mitochondrial function, redox balance, and nutrient sensing Ferroptosis represents an emerging metabolic vulnerability linking lipid peroxidation and glutathione metabolism Clinical translation of metabolic inhibitors faces challenges including toxicity, lack of biomarkers, and adaptive resistance Single-cell multi-omics and AI-driven approaches promise to enable metabolic subtyping for personalized therapy Similar content being viewed by others Background Non-small cell lung cancer (NSCLC) is the most prevalent type of lung cancer, accounting for approximately 85% of all lung cancer cases

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Arthropod cytosolic GSTs are mainly involved in xenobiotic adaptation

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Glutathione is a major antioxidant as the cofactor for glutathione peroxidase, one of the most important antioxidant enzymes in the body