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Regulation of the polarity protein Par6 by TGFbeta receptors controls epithelial cell plasticity.转化生长因子β受体对极性蛋白Par6的调控控制上皮细胞可塑性。
Science. 2005 Mar 11;307(5715):1603-9. doi: 10.1126/science.1105718.
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Type I transforming growth factor beta receptor binds to and activates phosphatidylinositol 3-kinase.I型转化生长因子β受体与磷脂酰肌醇3激酶结合并激活它。
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Smad4 silencing in pancreatic cancer cell lines using stable RNA interference and gene expression profiles induced by transforming growth factor-beta.利用稳定RNA干扰和转化生长因子-β诱导的基因表达谱在胰腺癌细胞系中沉默Smad4
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Smad4 deficiency in cervical carcinoma cells.子宫颈癌细胞中的Smad4缺陷
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Differential requirements for Smad4 in TGFbeta-dependent patterning of the early mouse embryo.Smad4在小鼠早期胚胎TGFβ依赖性模式形成中的差异需求。
Development. 2004 Aug;131(15):3501-12. doi: 10.1242/dev.01248. Epub 2004 Jun 23.
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PAI-1 expression is required for epithelial cell migration in two distinct phases of in vitro wound repair.在体外伤口修复的两个不同阶段,上皮细胞迁移需要PAI-1表达。
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New insights into TGF-beta-Smad signalling.转化生长因子-β-信号转导通路的新见解。
Trends Biochem Sci. 2004 May;29(5):265-73. doi: 10.1016/j.tibs.2004.03.008.
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Integration of Smad and forkhead pathways in the control of neuroepithelial and glioblastoma cell proliferation.Smad 信号通路与叉头框蛋白信号通路在调控神经上皮细胞和胶质母细胞瘤细胞增殖中的整合作用
Cell. 2004 Apr 16;117(2):211-23. doi: 10.1016/s0092-8674(04)00298-3.
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Integration of TGF-beta/Smad and Jagged1/Notch signalling in epithelial-to-mesenchymal transition.转化生长因子-β/ Smad信号通路与Jagged1/Notch信号通路在上皮-间质转化中的整合
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Smad4-independent regulation of p21/WAF1 by transforming growth factor-beta.转化生长因子-β对p21/WAF1的Smad4非依赖性调控
Oncogene. 2004 Feb 5;23(5):1043-51. doi: 10.1038/sj.onc.1207222.

Smad4依赖性定义了两类转化生长因子β(TGF-β)靶基因,并将TGF-β诱导的上皮-间质转化与其抗增殖和迁移反应区分开来。

Smad4 dependency defines two classes of transforming growth factor {beta} (TGF-{beta}) target genes and distinguishes TGF-{beta}-induced epithelial-mesenchymal transition from its antiproliferative and migratory responses.

作者信息

Levy Laurence, Hill Caroline S

机构信息

Laboratory of Developmental Signalling, Cancer Research UK London Research Institute, 44 Lincoln's Inn Fields, London WC2A 3PX, United Kingdom.

出版信息

Mol Cell Biol. 2005 Sep;25(18):8108-25. doi: 10.1128/MCB.25.18.8108-8125.2005.

DOI:10.1128/MCB.25.18.8108-8125.2005
PMID:16135802
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC1234333/
Abstract

In response to transforming growth factor beta (TGF-beta), Smad4 forms complexes with activated Smad2 and Smad3, which accumulate in the nucleus, where they both positively and negatively regulate TGF-beta target genes. Mutation or deletion of Smad4 is found in about 50% of pancreatic tumors and in about 15% of colorectal tumors. As Smad4 is a central component of the TGF-beta/Smad pathway, we have determined whether Smad4 is absolutely required for all TGF-beta responses, to evaluate the effect of its loss during human tumor development. We have generated cell lines from the immortalized human keratinocyte cell line HaCaT or the pancreatic tumor cell line Colo-357, which stably express a tetracyline-inducible small interfering RNA targeted against Smad4. In response to tetracycline, Smad4 expression is effectively silenced. Large-scale microarray analysis identifies two populations of TGF-beta target genes that are distinguished by their dependency on Smad4. Some genes absolutely require Smad4 for their regulation, while others do not. Functional analysis also indicates a differential Smad4 requirement for TGF-beta-induced functions; TGF-beta-induced cell cycle arrest and migration, but not epithelial-mesenchymal transition, are abolished after silencing of Smad4. Altogether our results suggest that loss of Smad4 might promote TGF-beta-mediated tumorigenesis by abolishing tumor-suppressive functions of TGF-beta while maintaining some tumor-promoting TGF-beta responses.

摘要

在对转化生长因子β(TGF-β)的应答中,Smad4与活化的Smad2和Smad3形成复合物,这些复合物在细胞核中积累,在细胞核中它们对TGF-β靶基因进行正调控和负调控。在约50%的胰腺肿瘤和约15%的结肠直肠肿瘤中发现了Smad4的突变或缺失。由于Smad4是TGF-β/Smad信号通路的核心组成部分,我们已确定Smad4对于所有TGF-β应答是否绝对必需,以评估其在人类肿瘤发生过程中缺失的影响。我们从永生化的人角质形成细胞系HaCaT或胰腺肿瘤细胞系Colo-357中生成了细胞系,这些细胞系稳定表达针对Smad4的四环素诱导型小干扰RNA。在四环素作用下,Smad4的表达被有效沉默。大规模微阵列分析确定了两类TGF-β靶基因,它们因其对Smad4的依赖性而有所区别。一些基因的调控绝对需要Smad4,而另一些则不需要。功能分析还表明,TGF-β诱导的功能对Smad4的需求存在差异;Smad4沉默后,TGF-β诱导的细胞周期停滞和迁移被消除,但上皮-间质转化未受影响。我们的结果总体表明,Smad4的缺失可能通过消除TGF-β的肿瘤抑制功能同时维持一些促进肿瘤的TGF-β应答来促进TGF-β介导的肿瘤发生。