Lipogenesis-driven EGFR palmitoylation enables metastatic immune evasion in triple-negative breast cancer.
This study reveals that de novo lipogenesis drives metastatic immune evasion in triple-negative breast cancer by promoting FASN-mediated EGFR palmitoylation, which sustains a lipid-dependent PI3K-AKT-mTOR signaling axis to suppress MHC-I antigen presentation and enable CD8+ T cell escape, a process that can be reversed by inhibiting FASN to restore anti-tumor immunity and block lung metastasis.