肿瘤相关巨噬细胞（TAM）在肿瘤微环境（TME）内经历代谢重编程，包括葡萄糖、氨基酸、脂肪酸代谢、三羧酸（TCA）循环、嘌呤代谢和自噬。 TAM和肿瘤细胞之间的代谢相互依赖性严重影响巨噬细胞的募集、分化、M2极化和上皮间质转化（EMT）相关因子的分泌，从而激活瘤内EMT通路并增强肿瘤细胞的侵袭和转移。肿瘤细胞代谢改变，包括缺氧、代谢物分泌、有氧代谢和自噬，影响TME的代谢景观，驱动巨噬细胞招募、分化、M2极化和代谢重编程，最终促进EMT、侵袭和转移。此外，巨噬细胞可以通过重新编程肿瘤细胞的有氧糖酵解来诱导肿瘤细胞 EMT。最近的实验和临床研究主要集中在巨噬细胞和肿瘤细胞之间的代谢相互作用，以控制转移和抑制肿瘤进展。本综述强调了 TAM 与肿瘤细胞代谢相关性在 EMT 中的调节作用，为高度转移性肿瘤的 TAM 靶向治疗提供了宝贵的见解。调节肿瘤和 TAM 之间的代谢相互作用代表了治疗转移性癌症患者的一种有前景的治疗策略。© 作者。

Tumor-associated macrophages (TAMs) undergo metabolic reprogramming, encompassing glucose, amino acid, fatty acid metabolism, tricarboxylic acid (TCA) cycle, purine metabolism, and autophagy, within the tumor microenvironment (TME). The metabolic interdependencies between TAMs and tumor cells critically influence macrophage recruitment, differentiation, M2 polarization, and secretion of epithelial-mesenchymal transition (EMT)-related factors, thereby activating intratumoral EMT pathways and enhancing tumor cell invasion and metastasis. Tumor cell metabolic alterations, including hypoxia, metabolite secretion, aerobic metabolism, and autophagy, affect the TME's metabolic landscape, driving macrophage recruitment, differentiation, M2 polarization, and metabolic reprogramming, ultimately facilitating EMT, invasion, and metastasis. Additionally, macrophages can induce tumor cell EMT by reprogramming their aerobic glycolysis. Recent experimental and clinical studies have focused on the metabolic interactions between macrophages and tumor cells to control metastasis and inhibit tumor progression. This review highlights the regulatory role of TAM-tumor cell metabolic codependencies in EMT, offering valuable insights for TAM-targeted therapies in highly metastatic tumors. Modulating the metabolic interplay between tumors and TAMs represents a promising therapeutic strategy for treating patients with metastatic cancers.© The author(s).