Ivaska Johanna
Medical Biotechnology; VTT Technical Research Centre of Finland; Turku Centre for Biotechnology and Department of Biochemistry and Food Chemistry; University of Turku; Turku, Finland.
Small GTPases. 2011 Jan;2(1):51-53. doi: 10.4161/sgtp.2.1.15114.
Epithelial-to-mesenchymal transition (EMT) is a critical event in the induction of cell motility and increased survival both under physiological situations like wound healing and during development as well as in malignant cells undergoing invasion and metastasis. Vimentin is an intermediate filament protein which is characteristically upregulated in cells undergoing EMT. For decades vimentin has been considered as a marker for EMT but its functional contribution to the process has remained unclear. Our data demonstrate that vimentin contributes to EMT via upregulating the gene expression of several EMT-linked genes. Especially, we find that vimentin regulates EMT associated induced migration via upregulation of the expression of receptor tyrosine kinase Axl. In addition to our data, several other exciting recent studies support the notion that vimentin in fact functions as a positive regulator of EMT and upregulation of vimentin appears to be a prerequisite for EMT induction.
上皮-间质转化(EMT)是诱导细胞迁移以及在诸如伤口愈合等生理状况下、发育过程中以及发生侵袭和转移的恶性细胞中提高细胞存活率的关键事件。波形蛋白是一种中间丝蛋白,在经历EMT的细胞中其特征性地上调。几十年来,波形蛋白一直被视为EMT的标志物,但其对该过程的功能贡献仍不清楚。我们的数据表明,波形蛋白通过上调几个与EMT相关基因的基因表达来促进EMT。特别是,我们发现波形蛋白通过上调受体酪氨酸激酶Axl的表达来调节与EMT相关的诱导迁移。除了我们的数据外,最近其他几项令人兴奋的研究也支持这样一种观点,即波形蛋白实际上作为EMT的正向调节因子发挥作用,并且波形蛋白的上调似乎是诱导EMT的先决条件。