增加的葡萄糖代谢和吸收是许多肿瘤的特点，临床上被用于诊断和监测癌症进展。除癌细胞外，肿瘤微环境（TME）包括广泛的基质、固有和适应性免疫细胞。这些细胞群体之间的合作和竞争支持肿瘤增殖、进展、转移和免疫逃避。细胞异质性导致代谢异质性，因为肿瘤内的代谢程序不仅取决于TME细胞组成，还取决于细胞状态、位置和营养素供应。除了促进癌细胞的代谢可塑性外，TME中改变的营养和信号还可以导致效应细胞的代谢免疫抑制和促进免疫调节细胞。本文讨论了TME内细胞的代谢编程如何促进肿瘤增殖、进展和转移。我们还讨论了如何针对代谢异质性提供治疗机会，以克服免疫抑制并增强免疫疗法。版权所有 ©2023 Elsevier Inc.。

Increased glucose metabolism and uptake are characteristic of many tumors and used clinically to diagnose and monitor cancer progression. In addition to cancer cells, the tumor microenvironment (TME) encompasses a wide range of stromal, innate, and adaptive immune cells. Cooperation and competition between these cell populations supports tumor proliferation, progression, metastasis, and immune evasion. Cellular heterogeneity leads to metabolic heterogeneity because metabolic programs within the tumor are dependent not only on the TME cellular composition but also on cell states, location, and nutrient availability. In addition to driving metabolic plasticity of cancer cells, altered nutrients and signals in the TME can lead to metabolic immune suppression of effector cells and promote regulatory immune cells. Here we discuss how metabolic programming of cells within the TME promotes tumor proliferation, progression, and metastasis. We also discuss how targeting metabolic heterogeneity may offer therapeutic opportunities to overcome immune suppression and augment immunotherapies.Copyright © 2023 Elsevier Inc. All rights reserved.