CDCP1 drives triple-negative breast cancer metastasis through reduction of lipid-droplet abundance and stimulation of fatty acid oxidation

Significance Approximately 34% of triple-negative breast cancer (TNBC) patients relapse with local recurrence or metastasis within 5 y of radiation and chemotherapy treatment. There are currently no targeted therapies to treat TNBC. This study offers therapeutic targets for blocking TNBC metastasis: cell-surface antigen CUB-domain containing protein 1 (CDCP1) and proteins in the lipid metabolism pathway. CDCP1 regulates lipid metabolism by reducing cytoplasmic lipid droplet abundance, stimulating fatty acid oxidation and oxidative phosphorylation. This metabolic pathway likely contributes to the energy production required for cell migration and metastasis of TNBC, and represents a potential therapeutic target.