These processes exert inhibitory or tumor-promoting effects on the activation, proliferation, differentiation and function of immune cells, forming a critical bridge linking tumor cell intrinsic metabolism and tumor immunity ( de novo serine synthesis pathway modulates the tumor immune microenvironment through metabolic reprogramming ( The balance between tumorigenesis and antitumor immune function governed by serine metabolism is determined by the abundance and activation status of distinct cell populations, as well as the expression profiles of various immune mediators and regulatory factors within the tumor microenvironment (TME) ( Bladder cancer cells with PSAT1 overexpression can secrete serine, which activates the PI3K/Akt pathway in macrophages and induces their polarization toward the M2 phenotype, thereby suppressing antitumor immune responses ( de novo serine synthesis promotes the production of -ketoglutarate, which activates the mTORC1 signaling pathway in macrophages, facilitates the acquisition of the M2 macrophage phenotype and sustains high PD-L1 expression, ultimately inhibiting the cytotoxic function of CD8 + T cells
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