Fig. 4: KRAS affects the TME by regulating lipid metabolism.

KRAS regulates the expression of genes involved in lipid metabolism, which significantly increases the accumulation of lipid metabolites in tumors. This accumulation impairs the T cell-mediated cytotoxicity, accelerates the pro-tumorigenic ability of CD4+FoxP3+ Treg cells, and promotes the secretion of CCL2 through the PPARδ activation. CCL2 recruits M2 macrophages, fostering an immunosuppressive TME.