代谢重构对癌症的发生和进展至关重要。我们以前曾表明，依赖于一碳代谢的甲酸产生经常超过癌细胞的合成需求，导致甲酸溢出。此外，我们也表明，增加的细胞外甲酸浓度促进了脑胶质母细胞瘤细胞的体外浸润能力。在这里，我们用体外和体内实验来证实这些初步观察结果。我们还表明，暴露于外源性甲酸可以使癌细胞增加对侵袭表型的启动，从而在体内形成更多的转移瘤。我们的结果表明，肿瘤微环境内局部甲酸浓度的增加可能是促进转移的一个因素。此外，我们还描述了甲酸依赖的增强侵袭性与脂质代谢和基质金属蛋白酶活性适应之间的机制相互作用。我们的发现巩固了甲酸作为促进侵袭代谢产物的作用，并有需要进一步研究以更好地理解甲酸与脂质代谢之间的相互作用。版权所有 © 2023 作者。Elsevier Inc. 发行，保留所有版权。

Metabolic rewiring is essential for cancer onset and progression. We previously showed that one-carbon metabolism-dependent formate production often exceeds the anabolic demand of cancer cells, resulting in formate overflow. Furthermore, we showed that increased extracellular formate concentrations promote the in vitro invasiveness of glioblastoma cells. Here, we substantiate these initial observations with ex vivo and in vivo experiments. We also show that exposure to exogeneous formate can prime cancer cells toward a pro-invasive phenotype leading to increased metastasis formation in vivo. Our results suggest that the increased local formate concentration within the tumor microenvironment can be one factor to promote metastases. Additionally, we describe a mechanistic interplay between formate-dependent increased invasiveness and adaptations of lipid metabolism and matrix metalloproteinase activity. Our findings consolidate the role of formate as pro-invasive metabolite and warrant further research to better understand the interplay between formate and lipid metabolism.Copyright © 2023 The Authors. Published by Elsevier Inc. All rights reserved.