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本文引用的文献

1
Vimentin regulates EMT induction by Slug and oncogenic H-Ras and migration by governing Axl expression in breast cancer.波形蛋白通过调控 Slug 和致癌性 H-Ras 诱导 EMT 发生以及调控 Axl 表达进而调控乳腺癌的迁移。
Oncogene. 2011 Mar 24;30(12):1436-48. doi: 10.1038/onc.2010.509. Epub 2010 Nov 8.
2
Vimentin is a novel AKT1 target mediating motility and invasion.波形蛋白是一种新型 AKT1 靶标,介导运动和侵袭。
Oncogene. 2011 Jan 27;30(4):457-70. doi: 10.1038/onc.2010.421. Epub 2010 Sep 20.
3
Keeping the vimentin network under control: cell-matrix adhesion-associated plectin 1f affects cell shape and polarity of fibroblasts.保持中间丝网络的控制:细胞-基质黏附相关网蛋白 1f 影响成纤维细胞的形态和极性。
Mol Biol Cell. 2010 Oct 1;21(19):3362-75. doi: 10.1091/mbc.E10-02-0094. Epub 2010 Aug 11.
4
An anti-Axl monoclonal antibody attenuates xenograft tumor growth and enhances the effect of multiple anticancer therapies.一种抗 Axl 的单克隆抗体可减弱异种移植肿瘤的生长,并增强多种抗癌疗法的效果。
Oncogene. 2010 Sep 23;29(38):5254-64. doi: 10.1038/onc.2010.268. Epub 2010 Jul 5.
5
ERK2 but not ERK1 induces epithelial-to-mesenchymal transformation via DEF motif-dependent signaling events.ERK2 而非 ERK1 通过 DEF 基序依赖性信号事件诱导上皮-间充质转化。
Mol Cell. 2010 Apr 9;38(1):114-27. doi: 10.1016/j.molcel.2010.02.020.
6
R428, a selective small molecule inhibitor of Axl kinase, blocks tumor spread and prolongs survival in models of metastatic breast cancer.R428 是一种选择性的 Axl 激酶小分子抑制剂,可阻止转移性乳腺癌模型中的肿瘤扩散并延长生存期。
Cancer Res. 2010 Feb 15;70(4):1544-54. doi: 10.1158/0008-5472.CAN-09-2997. Epub 2010 Feb 9.
7
Vimentin induces changes in cell shape, motility, and adhesion during the epithelial to mesenchymal transition.波形蛋白在上皮细胞向间充质转化过程中诱导细胞形态、运动和黏附的改变。
FASEB J. 2010 Jun;24(6):1838-51. doi: 10.1096/fj.09-151639. Epub 2010 Jan 22.
8
Axl is an essential epithelial-to-mesenchymal transition-induced regulator of breast cancer metastasis and patient survival.Axl 是乳腺癌转移和患者生存的上皮-间充质转化诱导调节因子。
Proc Natl Acad Sci U S A. 2010 Jan 19;107(3):1124-9. doi: 10.1073/pnas.0909333107. Epub 2009 Dec 28.
9
Vimentin regulates scribble activity by protecting it from proteasomal degradation.波形蛋白通过保护scribble免受蛋白酶体降解来调节其活性。
Mol Biol Cell. 2009 Jun;20(12):2841-55. doi: 10.1091/mbc.e08-02-0199. Epub 2009 Apr 22.
10
TAM receptor tyrosine kinases: biologic functions, signaling, and potential therapeutic targeting in human cancer.TAM受体酪氨酸激酶:生物学功能、信号传导及在人类癌症中的潜在治疗靶点
Adv Cancer Res. 2008;100:35-83. doi: 10.1016/S0065-230X(08)00002-X.

波形蛋白:上皮-间质转化诱导中的核心枢纽?

Vimentin: Central hub in EMT induction?

作者信息

Ivaska Johanna

机构信息

Medical Biotechnology; VTT Technical Research Centre of Finland; Turku Centre for Biotechnology and Department of Biochemistry and Food Chemistry; University of Turku; Turku, Finland.

出版信息

Small GTPases. 2011 Jan;2(1):51-53. doi: 10.4161/sgtp.2.1.15114.

DOI:10.4161/sgtp.2.1.15114
PMID:21686283
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC3116616/
Abstract

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.

摘要

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。