Department of Biochemistry, Interdisciplinary Graduate School of Medicine and Engineering, University of Yamanashi, Chuo, Yamanashi, Japan.
J Biochem. 2012 Jun;151(6):563-71. doi: 10.1093/jb/mvs040. Epub 2012 Apr 23.
Epithelial-mesenchymal transition (EMT) is a crucial event in appropriate embryonic development as well as in wound healing, tissue repair and cancer progression in adult tissues. EMT endows cells with migratory and invasive properties, inhibits apoptosis and senescence, contributes to immunosuppression and induces stress resistance and stem cell properties. Many secreted polypeptide factors act in a sequential or cooperative manner to elicit EMT. Transforming growth factor (TGF)-β can initiate and maintain EMT by activating intracellular signalling pathways. Recent studies have provided new insights into molecular mechanisms by which TGF-β mediates changes in transcription of EMT regulators and EMT marker proteins, as well as changes in alternative splicing controlled by epithelial splicing regulatory proteins 1 and 2. Here, we present some of the emerging molecular mechanisms that mediate EMT upon exposure to TGF-β.
上皮-间充质转化(EMT)是胚胎发育、创伤愈合、组织修复以及成人组织中癌症进展过程中的一个关键事件。EMT 赋予细胞迁移和侵袭特性,抑制细胞凋亡和衰老,有助于免疫抑制,并诱导应激耐受和干细胞特性。许多分泌的多肽因子以顺序或协同的方式发挥作用,引发 EMT。转化生长因子(TGF)-β 通过激活细胞内信号通路,引发和维持 EMT。最近的研究提供了新的见解,阐明了 TGF-β 如何调节 EMT 调控因子和 EMT 标志物蛋白转录的分子机制,以及上皮剪接调节蛋白 1 和 2 控制的选择性剪接变化。在这里,我们介绍了一些 EMT 发生的新兴分子机制,这些机制在 TGF-β 暴露下发挥作用。