The tumor microenvironment (TME) is a complex system composed of tumor cells, stromal cells, and non-cellular components. Tumor cells employ metabolic reprogramming to alter the TME, creating an immunosuppressive environment that promotes immune evasion. This review highlights the impact of altered glucose, amino acid, and lipid metabolism in the TME on the function and differentiation of non-tumor cells, such as regulatory T-cells (Tregs) and myeloid-derived suppressor cells (MDSCs). Metabolic reprogramming in tumor cells, particularly through glycolysis, amino acid, and lipid metabolism, affects immune cell function and differentiation. For example, hyperglycolysis in tumor cells can increase immunosuppressive metabolites and reduce immunostimulatory molecules, inhibiting T-cell recruitment and function. Additionally, tumor cells upregulate amino acid uptake, particularly L-glutamine, which is crucial for cancer cell growth. This competition for nutrients impairs the function of anti-tumor immune cells, promoting immune evasion. Lipid metabolic disorders, involving fatty acids and cholesterol, are also key metabolic changes in tumor cell proliferation. Excessive lipid accumulation in the TME can suppress anti-tumor immunity and promote the redifferentiation of immune cells into tumor-promoting phenotypes. The review discusses the metabolic reprogramming of various immune cells, including dendritic cells (DCs), effector T-cells, and natural killer (NK) cells, and how these changes impact their function and anti-tumor activity. Targeting the metabolic pathways of tumor cells and immune cells represents a promising approach in cancer therapy, with potential to enhance the efficacy of immunotherapies.The tumor microenvironment (TME) is a complex system composed of tumor cells, stromal cells, and non-cellular components. Tumor cells employ metabolic reprogramming to alter the TME, creating an immunosuppressive environment that promotes immune evasion. This review highlights the impact of altered glucose, amino acid, and lipid metabolism in the TME on the function and differentiation of non-tumor cells, such as regulatory T-cells (Tregs) and myeloid-derived suppressor cells (MDSCs). Metabolic reprogramming in tumor cells, particularly through glycolysis, amino acid, and lipid metabolism, affects immune cell function and differentiation. For example, hyperglycolysis in tumor cells can increase immunosuppressive metabolites and reduce immunostimulatory molecules, inhibiting T-cell recruitment and function. Additionally, tumor cells upregulate amino acid uptake, particularly L-glutamine, which is crucial for cancer cell growth. This competition for nutrients impairs the function of anti-tumor immune cells, promoting immune evasion. Lipid metabolic disorders, involving fatty acids and cholesterol, are also key metabolic changes in tumor cell proliferation. Excessive lipid accumulation in the TME can suppress anti-tumor immunity and promote the redifferentiation of immune cells into tumor-promoting phenotypes. The review discusses the metabolic reprogramming of various immune cells, including dendritic cells (DCs), effector T-cells, and natural killer (NK) cells, and how these changes impact their function and anti-tumor activity. Targeting the metabolic pathways of tumor cells and immune cells represents a promising approach in cancer therapy, with potential to enhance the efficacy of immunotherapies.