Functional interaction of E1AF and sp1 in glioma invasion
Functional interaction of E1AF and sp1 in glioma invasion
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E1AF 和 sp1 在神经胶质瘤侵袭中的功能相互作用
DOI：
10.1128/mcb.02302-06
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发表时间：
2007-12-01
影响因子：
5.3
通讯作者：
Gu, Jianxin
中科院分区：
文献类型：
--
作者：
Jiang, Jianhai;Wei, Yuanyan;Gu, Jianxin
转录因子E1AF广为人知的是通过直接结合参与肿瘤迁移和侵袭的基因启动子在肿瘤转移中发挥关键作用。在此，我们首次报道E1AF是一种与广泛表达的Sp1转录因子新的结合伴侣。E1AF与Sp1形成复合物，有助于Sp1的磷酸化和转录活性，并作为表皮生长因子与Sp1磷酸化和活性之间的中介物发挥作用。Sp1作为载体将E1AF带到启动子区域，从而激活与胶质瘤相关的β1 - 4 - 半乳糖基转移酶V（GalT V；EC 2.4.1.38）基因的转录。在生物学上，E1AF与Sp1协同作用，部分通过上调GalT V，在胶质瘤中作为一种正向侵袭调节因子发挥作用。本报告描述了一种涉及E1AF和Sp1转录因子协同作用的胶质瘤侵袭新机制。
Transcription factor E1AF is widely known to play critical roles in tumor metastasis via directly binding to the promoters of genes involved in tumor migration and invasion. Here, we report for the first time E1AF as a novel binding partner for ubiquitously expressed Sp1 transcription factor. E1AF forms a complex with Sp1, contributes to Sp1 phosphorylation and transcriptional activity, and functions as a mediator between epidermal growth factor and Sp1 phosphorylation and activity. Sp1 functions as a carrier bringing E1AF to the promoter region, thus activating transcription of glioma-related gene for PI,beta 1-4-galactosyltransferase V (GalT V; EC 2.4.1.38). Biologically, E1AF functions as a positive invasion regulator in glioma in cooperation with Sp1 partly via up-regulation of GalT V. This report describes a new mechanism of glioma invasion involving a cooperative effort between E1AF and Sp1 transcription factors.