Serrano-Gomez Silvia Juliana, Maziveyi Mazvita, Alahari Suresh K
Department of Biochemistry and Molecular Biology, LSUHSC School of Medicine, New Orleans, LA, 70112, USA.
Pontificia Universidad Javeriana, Bogota, Colombia.
Mol Cancer. 2016 Feb 24;15:18. doi: 10.1186/s12943-016-0502-x.
The epithelial to mesenchymal transition (EMT) is a biological process in which a non-motile epithelial cell changes to a mesenchymal phenotype with invasive capacities. This phenomenon has been well documented in multiple biological processes including embryogenesis, fibrosis, tumor progression and metastasis. The hallmark of EMT is the loss of epithelial surface markers, most notably E-cadherin, and the acquisition of mesenchymal markers including vimentin and N-cadherin. The downregulation of E-cadherin during EMT can be mediated by its transcriptional repression through the binding of EMT transcription factors (EMT-TFs) such as SNAIL, SLUG and TWIST to E-boxes present in the E-cadherin promoter. Additionally, EMT-TFs can also cooperate with several enzymes to repress the expression of E-cadherin and regulate EMT at the epigenetic and post- translational level. In this review, we will focus on epigenetic and post- translational modifications that are important in EMT. In addition, we will provide an overview of the various therapeutic approaches currently being investigated to undermine EMT and hence, the metastatic progression of cancer as well.
上皮-间质转化（EMT）是一个生物学过程，在此过程中，非运动性的上皮细胞转变为具有侵袭能力的间充质表型。这种现象在包括胚胎发生、纤维化、肿瘤进展和转移在内的多个生物学过程中都有充分记录。EMT的标志是上皮表面标志物的丧失，最显著的是E-钙黏蛋白，以及获得包括波形蛋白和N-钙黏蛋白在内的间充质标志物。EMT过程中E-钙黏蛋白的下调可通过EMT转录因子（EMT-TFs）如SNAIL、SLUG和TWIST与E-钙黏蛋白启动子中存在的E盒结合而导致其转录抑制来介导。此外，EMT-TFs还可与多种酶协同作用，在表观遗传和翻译后水平抑制E-钙黏蛋白的表达并调节EMT。在本综述中，我们将重点关注在EMT中重要的表观遗传和翻译后修饰。此外，我们还将概述目前正在研究的各种治疗方法，这些方法旨在破坏EMT，从而抑制癌症的转移进程。
