Cancer cells are well-known for adapting their metabolism to maintain high proliferation rates and survive in unfavorable environments with low oxygen and nutritional deficiency. Metabolic reprogramming most commonly arises from the tumor microenvironment (TME). The events of metabolic pathways include the Warburg effect, shift in Krebs cycle metabolites, and increase rate of oxidative phosphorylation that provides the energy for the development and invasion of cancer cells. The TME and shift in tumor metabolism shows a close relationship through bidirectional signaling pathways between the stromal and tumor cells. Cancer-associated fibroblasts (CAFs) are the main type of stromal cells in the TME and consist of a heterogeneous and plastic population that play key roles in tumor growth and metastatic capacity. Emerging evidence suggests that CAFs act as major regulators in shaping tumor metabolism especially through the dysregulation of several metabolic pathways, including glucose, amino acid, and lipid metabolism. The arrangement of these metabolic switches is believed to shape distinct CAF behavior and change tumor cell behavior by the CAFs. The crosstalk between cancer cells and CAFs is associated with cell metabolic reprogramming that contributes to cancer cell growth, progression, and evasion from cancer therapies. But the mechanism and process of this interaction remain unclear. This review aimed to highlight the metabolic couplings between tumor cells and CAFs. We reviewed the recent literature supporting an important role of CAFs in the regulation of cancer cell metabolism, and the relevant pathways, which may serve as targets for therapeutic interventions.

中文翻译：

---

癌症相关成纤维细胞的代谢重编程及其对癌细胞重编程的影响

癌细胞以适应其新陈代谢以维持高增殖率并在低氧和营养缺乏的不利环境中生存而闻名。代谢重编程最常见于肿瘤微环境 (TME)。代谢途径的事件包括 Warburg 效应、克雷布斯循环代谢物的转变以及为癌细胞的发育和侵袭提供能量的氧化磷酸化速率的增加。TME和肿瘤代谢的转变通过基质细胞和肿瘤细胞之间的双向信号通路显示出密切的关系。癌症相关成纤维细胞 (CAF) 是 TME 中基质细胞的主要类型，由在肿瘤生长和转移能力中起关键作用的异质性和可塑性群体组成。新出现的证据表明，CAF 是塑造肿瘤代谢的主要调节剂，特别是通过几种代谢途径的失调，包括葡萄糖、氨基酸和脂质代谢。这些代谢开关的排列被认为塑造了不同的 CAF 行为并通过 CAF 改变了肿瘤细胞的行为。癌细胞和 CAF 之间的串扰与细胞代谢重编程有关，这有助于癌细胞生长、进展和逃避癌症治疗。但这种相互作用的机制和过程仍不清楚。本综述旨在强调肿瘤细胞和 CAF 之间的代谢耦合。我们回顾了最近支持 CAF 在调节癌细胞代谢中的重要作用的文献，以及相关途径，