Metabolic reprogramming and immune evasion: the interplay in the tumor microenvironment Tumor cells evade immune surveillance through metabolic reprogramming, altering the tumor microenvironment (TME) to modulate immune cell functions. When a tumor is immunogenic, it activates cytotoxic T-cells to destroy it, but tumors adapt by manipulating glucose, amino acid, and lipid metabolism to create an immunosuppressive TME. These metabolic changes impact non-tumor cells, such as inhibiting effector T-cells while expanding regulatory T-cells and myeloid-derived suppressor cells. Additionally, they disrupt cytokine and chemokine secretion, enhancing immunosuppression. Research increasingly focuses on the regulatory roles of non-tumor cells in the TME, evaluating how their reprogrammed metabolism influences immune evasion. Despite incomplete understanding of tumor and non-tumor cell metabolic interactions, these elements pose significant challenges for cancer immunotherapy. This review highlights the impact of altered glucose, amino acid, and lipid metabolism in the TME on non-tumor cell metabolism and function, providing new insights for developing novel cancer immunotherapies. The TME is an environmental system composed of tumor cells, stromal cells, and non-cellular components. Due to high metabolic activity, poor vascularization, and increased inflammation, the TME becomes dysregulated, characterized by hypoxia, metabolic dysregulation, high lactic acid levels, and immunosuppression. Stromal cells include cancer-associated fibroblasts (CAFs) and endothelial cells, which promote tumor growth and angiogenesis. Immune cells, including lymphocytes, tumor-associated macrophages (TAMs), dendritic cells (DCs), natural killer (NK) cells, regulatory T-cells (Tregs), and myeloid-derived suppressor cells (MDSCs), play crucial roles in immune surveillance, homeostasis, immune defense, and tumor development. Tumor cells undergo metabolic reprogramming, a hallmark of tumor initiation and progression. Non-tumor cells in the TME also undergo metabolic reprogramming, which impacts tumor immune evasion. Cell metabolism significantly influences immune cell function, and immune cell metabolic reprogramming enhances their function, essential for tumor immune responses. Immune cell activation requires large amounts of energy and metabolic intermediates for biosynthesis and antibody effector functions. Activated anti-tumor immune cells have metabolic patterns similar to tumor cells, leading to competition within the TME. Tumor cells have distinct metabolic reprogramming pathways and various oncogene mutations, making them key competitors for TME nutrients. Metabolites produced by tumor cells regulate immune cell activation, differentiation, and function. Tumor hyperglycolysis can trigger PD-L1 expression on the cell surface and induce mutations in the tumor suppressor gene P53. Glioblastoma cell studies show that elevated HK2 expression under high glucose conditions promotes NF-κB activation, increasing PD-L1 expressionMetabolic reprogramming and immune evasion: the interplay in the tumor microenvironment Tumor cells evade immune surveillance through metabolic reprogramming, altering the tumor microenvironment (TME) to modulate immune cell functions. When a tumor is immunogenic, it activates cytotoxic T-cells to destroy it, but tumors adapt by manipulating glucose, amino acid, and lipid metabolism to create an immunosuppressive TME. These metabolic changes impact non-tumor cells, such as inhibiting effector T-cells while expanding regulatory T-cells and myeloid-derived suppressor cells. Additionally, they disrupt cytokine and chemokine secretion, enhancing immunosuppression. Research increasingly focuses on the regulatory roles of non-tumor cells in the TME, evaluating how their reprogrammed metabolism influences immune evasion. Despite incomplete understanding of tumor and non-tumor cell metabolic interactions, these elements pose significant challenges for cancer immunotherapy. This review highlights the impact of altered glucose, amino acid, and lipid metabolism in the TME on non-tumor cell metabolism and function, providing new insights for developing novel cancer immunotherapies. The TME is an environmental system composed of tumor cells, stromal cells, and non-cellular components. Due to high metabolic activity, poor vascularization, and increased inflammation, the TME becomes dysregulated, characterized by hypoxia, metabolic dysregulation, high lactic acid levels, and immunosuppression. Stromal cells include cancer-associated fibroblasts (CAFs) and endothelial cells, which promote tumor growth and angiogenesis. Immune cells, including lymphocytes, tumor-associated macrophages (TAMs), dendritic cells (DCs), natural killer (NK) cells, regulatory T-cells (Tregs), and myeloid-derived suppressor cells (MDSCs), play crucial roles in immune surveillance, homeostasis, immune defense, and tumor development. Tumor cells undergo metabolic reprogramming, a hallmark of tumor initiation and progression. Non-tumor cells in the TME also undergo metabolic reprogramming, which impacts tumor immune evasion. Cell metabolism significantly influences immune cell function, and immune cell metabolic reprogramming enhances their function, essential for tumor immune responses. Immune cell activation requires large amounts of energy and metabolic intermediates for biosynthesis and antibody effector functions. Activated anti-tumor immune cells have metabolic patterns similar to tumor cells, leading to competition within the TME. Tumor cells have distinct metabolic reprogramming pathways and various oncogene mutations, making them key competitors for TME nutrients. Metabolites produced by tumor cells regulate immune cell activation, differentiation, and function. Tumor hyperglycolysis can trigger PD-L1 expression on the cell surface and induce mutations in the tumor suppressor gene P53. Glioblastoma cell studies show that elevated HK2 expression under high glucose conditions promotes NF-κB activation, increasing PD-L1 expression