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Preclinical research links it to three main mechanisms: VEGFR2/eNOS angiogenic signaling, Src-caveolin-1-eNOS nitric oxide modulation, and FAK/paxillin cell-migration signaling

Moreover, intracellular lipid accumulation or supplementation with exogenous fatty acids can trigger the generation of reactive oxygen species (ROS) and the secretion of immunosuppressive cytokines, thereby facilitating the polarization of macrophages toward a pro-tumorigenic M2 phenotype, which in turn enhances tumor cell invasiveness and metastatic potential (87)