癌症发病率和死亡率正在增加，并影响着全球的预期寿命。肿瘤微环境（TME）中的代谢重编程与肿瘤的发生、进展、转移和耐药性密切相关。肿瘤细胞通过细胞因子和代谢物的代谢诱导以及代谢底物竞争来驱动 TME 中其他细胞的代谢重编程。因此，这通过提供代谢支持并促进免疫抑制和血管生成来促进肿瘤细胞生长。 TME 中的代谢相互作用提供了潜在的治疗靶点。在这里，我们重点关注 TME 中四个主要细胞亚群的代谢重编程：CAF、TAM、TIL 和 TEC，以及它们与肿瘤细胞的相互作用。我们还总结了针对这些细胞代谢途径的药物和疗法，特别是在免疫检查点阻断疗法的背景下。版权所有 © 2024。由 Elsevier B.V. 出版。

Cancer incidence and mortality are increasing and impacting global life expectancy. Metabolic reprogramming in the tumor microenvironment (TME) is intimately related to tumorigenesis, progression, metastasis and drug resistance. Tumor cells drive metabolic reprogramming of other cells in the TME through metabolic induction of cytokines and metabolites, and metabolic substrate competition. Consequently, this boosts tumor cell growth by providing metabolic support and facilitating immunosuppression and angiogenesis. The metabolic interplay in the TME presents potential therapeutic targets. Here, we focus on the metabolic reprogramming of four principal cell subsets in the TME: CAFs, TAMs, TILs and TECs, and their interaction with tumor cells. We also summarize medications and therapies targeting these cells' metabolic pathways, particularly in the context of immune checkpoint blockade therapy.Copyright © 2024. Published by Elsevier B.V.