Sciacovelli Marco, Frezza Christian
Medical Research Council Cancer Unit, Hutchison/MRC Research Centre, University of Cambridge, UK.
FEBS J. 2017 Oct;284(19):3132-3144. doi: 10.1111/febs.14090. Epub 2017 May 21.
Several lines of evidence indicate that during transformation epithelial cancer cells can acquire mesenchymal features via a process called epithelial-to-mesenchymal transition (EMT). This process endows cancer cells with increased invasive and migratory capacity, enabling tumour dissemination and metastasis. EMT is associated with a complex metabolic reprogramming, orchestrated by EMT transcription factors, which support the energy requirements of increased motility and growth in harsh environmental conditions. The discovery that mutations in metabolic genes such as FH, SDH and IDH activate EMT provided further evidence that EMT and metabolism are intertwined. In this review, we discuss the role of EMT in cancer and the underpinning metabolic reprogramming. We also put forward the hypothesis that, by altering chromatin structure and function, metabolic pathways engaged by EMT are necessary for its full activation.
多条证据表明，在肿瘤转化过程中，上皮癌细胞可通过一种称为上皮-间质转化（EMT）的过程获得间质特征。这一过程赋予癌细胞更强的侵袭和迁移能力，促使肿瘤扩散和转移。EMT与复杂的代谢重编程相关，由EMT转录因子精心调控，以满足在恶劣环境条件下增强的运动性和生长对能量的需求。代谢基因如FH、SDH和IDH的突变可激活EMT，这一发现进一步证明了EMT与代谢相互交织。在本综述中，我们讨论了EMT在癌症中的作用以及相关的代谢重编程。我们还提出假说，即通过改变染色质结构和功能，EMT所涉及的代谢途径对于其完全激活是必要的。
