代谢重编程被认为是癌症的核心特征，其中脂质的过度积累促进了癌症的发生、进展和转移。脂质代谢通常被视为膳食脂肪的消化和吸收过程，癌细胞利用脂质的方式通常受到肿瘤微环境内复杂相互作用的影响。在多种癌症风险因素中，肥胖与多种癌症类型呈正相关，而如限制热量摄入和禁食等饮食有助于改善健康并延缓癌症进展。尽管肿瘤微环境具有异质性，这些饮食对肿瘤发生或癌症预防的影响通常是在癌细胞上进行研究的。癌细胞经常与这些异质微环境成分进行互动，包括免疫细胞和基质细胞，以促进癌症的进展和转移，这些区域之间存在着复杂的代谢相互作用。在这里，我们着重讨论肿瘤微环境中的脂质代谢和对膳食脂肪的响应，重点放在免疫和基质组分上，并为围绕脂质代谢和信号通路的治疗策略照明。Copyright © 2023. Elsevier B.V.出版。

Metabolic reprogramming has been considered a core hallmark of cancer, in which excessive accumulation of lipids promote cancer initiation, progression and metastasis. Lipid metabolism is often considered as the digestion and absorption process of dietary fat, and the ways in which cancer cells utilize lipids are often influenced by the complex interactions within the tumor microenvironment. Among multiple cancer risk factors, obesity has a positive association with multiple cancer types, while diets like calorie restriction and fasting improve health and delay cancer. Impact of these diets on tumorigenesis or cancer prevention are generally studied on cancer cells, despite heterogeneity of the tumor microenvironment. Cancer cells regularly interact with these heterogeneous microenvironmental components, including immune and stromal cells, to promote cancer progression and metastasis, and there is an intricate metabolic crosstalk between these compartments. Here, we focus on discussing fat metabolism and response to dietary fat in the tumor microenvironment, focusing on both immune and stromal components and shedding light on therapeutic strategies surrounding lipid metabolic and signaling pathways.Copyright © 2023. Published by Elsevier B.V.