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MCB Accepts, published online ahead of print on 15 October 2007
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Mol. Cell. Biol. doi:10.1128/MCB.02302-06
Copyright (c) 2007, American Society for Microbiology and/or the Listed Authors/Institutions. All Rights Reserved.

Functional Interaction of E1AF and Sp1 in Glioma Invasion

Jianhai Jiang, Yuanyan Wei, Jialin Shen, Dan Liu, Xiaoning Chen, Jin Zhou, Hongliang Zong, Xiaojin Yun, Xiangfei Kong, Si Zhang, Yanzhong Yang, and Jianxin Gu*

Key Laboratory of Medical Molecular Virology Ministry of Education and Health, Gene Research Center, Shanghai Medical College and Institutes of Biomedical Sciences of Fudan University, Shanghai 200032, PR China

* To whom correspondence should be addressed. Email: jxgu{at}shmu.edu.cn.


   Abstract

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 that E1AF as a novel binding partner for ubiquitously expressed Sp1 transcription factor. E1AF forms a complex with Sp1, contributes in 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 {beta}1, 4-galactosyltransferase V (GalT V; 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 study describes a new mechanism of glioma invasion involving a cooperation effort of E1AF and Sp1 transcription factors.




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