To explore the role of CD36-mediated fatty acid oxidation in immune evasion and metastasis in NSCLC.
Analyzed CD36 expression in circulating tumor cells (CTCs)
Assessed metabolic reprogramming linked to fatty acid oxidation
Examined immune response in PD-1-resistant NSCLC
Identified CD36+ CTCs as a driver of immune evasion
Demonstrated fatty acid oxidation as a key metabolic pathway
Suggested that targeting this pathway may improve immunotherapy outcomes
Abstract
CD36+ CTCs drive immune evasion and metastasis in PD-1-resistant NSCLC through FAO-dependent metabolic reprogramming. Targeting this metabolic vulnerability may enhance the efficacy of immunotherapy.