Center for Theoretical Biological Physics, Rice University, Houston, TX, USA.
Department of Molecular and Human Genetics, Baylor College of Medicine, Houston, TX, USA.
Br J Cancer. 2021 Jun;124(12):1902-1911. doi: 10.1038/s41416-021-01385-y. Epub 2021 Apr 15.
Cancer cells have the plasticity to adjust their metabolic phenotypes for survival and metastasis. A developmental programme known as epithelial-to-mesenchymal transition (EMT) plays a critical role during metastasis, promoting the loss of polarity and cell-cell adhesion and the acquisition of motile, stem-cell characteristics. Cells undergoing EMT or the reverse mesenchymal-to-epithelial transition (MET) are often associated with metabolic changes, as the change in phenotype often correlates with a different balance of proliferation versus energy-intensive migration. Extensive crosstalk occurs between metabolism and EMT, but how this crosstalk leads to coordinated physiological changes is still uncertain. The elusive connection between metabolism and EMT compromises the efficacy of metabolic therapies targeting metastasis. In this review, we aim to clarify the causation between metabolism and EMT on the basis of experimental studies, and propose integrated theoretical-experimental efforts to better understand the coupled decision-making of metabolism and EMT.
癌细胞具有调整代谢表型以生存和转移的可塑性。一种被称为上皮-间充质转化（EMT）的发育程序在转移过程中起着关键作用，促进极性和细胞-细胞黏附的丧失以及运动性、干细胞特征的获得。经历 EMT 或相反的间充质-上皮转化（MET）的细胞通常与代谢变化相关，因为表型的变化通常与增殖与能量密集型迁移之间的不同平衡相关。代谢和 EMT 之间会发生广泛的串扰，但这种串扰如何导致协调的生理变化尚不确定。代谢和 EMT 之间难以捉摸的联系削弱了针对转移的代谢治疗的疗效。在这篇综述中，我们旨在根据实验研究阐明代谢与 EMT 之间的因果关系，并提出综合的理论-实验努力，以更好地理解代谢和 EMT 的耦合决策。
