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Molecular and Cellular Biology, December 2007, p. 8770-8782, Vol. 27, No. 24
0270-7306/07/$08.00+0 doi:10.1128/MCB.02302-06
Copyright © 2007, American Society for Microbiology. All Rights Reserved.

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, People's Republic of China
Received 9 December 2006/ Returned for modification 16 January 2007/ Accepted 24 September 2007
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 ß1,4-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.
Published ahead of print on 15 October 2007.
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