Metastasis is the most frequent cause of death in cancer patients. Epithelial-to-mesenchymal transition (EMT) is the process in which cells lose epithelial integrity and become motile, a critical step for cancer cell invasion, drug resistance and immune evasion. The transforming growth factor-β (TGFβ) signaling pathway is a major driver of EMT. Increasing evidence demonstrates that metabolic reprogramming is a hallmark of cancer and extensive metabolic changes are observed during EMT. The aim of this review is to summarize and interconnect recent findings that illustrate how changes in glycolysis, mitochondrial, lipid and choline metabolism coincide and functionally contribute to TGFβ-induced EMT. We describe TGFβ signaling is involved in stimulating both glycolysis and mitochondrial respiration. Interestingly, the subsequent metabolic consequences for the redox state and lipid metabolism in cancer cells are found to be in favor of EMT as well. Combined we illustrate that a better understanding of the mechanistic links between TGFβ signaling, cancer metabolism and EMT holds promising strategies for cancer therapy, some of which are already actively being explored in the clinic.

转移是癌症患者最常见的死亡原因。上皮间质转化（EMT）是细胞失去上皮完整性并变得能动的过程，是癌细胞侵袭、耐药和免疫逃避的关键步骤。转化生长因子-β (TGFβ) 信号通路是 EMT 的主要驱动因素。越来越多的证据表明，代谢重编程是癌症的一个标志，并且在 EMT 期间观察到广泛的代谢变化。本综述的目的是总结和互连最近的发现，这些发现说明了糖酵解、线粒体、脂质和胆碱代谢的变化如何一致并在功能上促进 TGFβ 诱导的 EMT。我们描述了 TGFβ 信号传导参与刺激糖酵解和线粒体呼吸。有趣的是，随后发现癌细胞氧化还原状态和脂质代谢的代谢结果也有利于 EMT。结合起来，我们表明，更好地了解 TGFβ 信号传导、癌症代谢和 EMT 之间的机制联系为癌症治疗提供了有希望的策略，其中一些策略已经在临床中积极探索。