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First published online 11 December 2002
doi: 10.1242/jcs.00224
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Research Article |
1 Instituto de Investigaciones Biomédicas "Alberto Sols"
(CSIC-UAM), Arturo Duperier, 4, 28029 Madrid, Spain
2 Centro Nacional de Investigaciones Oncológicas, Melchor
Fernández Almagro, 4, 28029 Madrid, Spain
* Present address: Laboratory of Mammalian Cell Biology and Development, The
Rockefeller University. 1230 York Avenue, Box 300. New York, NY 10021,
USA
Author for correspondence (e-mail:
acano{at}iib.uam.es)
Accepted 14 October 2002
Transcriptional repression mechanisms have emerged as one of the crucial processes for the downregulation of E-cadherin expression during development and tumour progression. Recently, several E-cadherin transcriptional repressors have been characterized (Snail, E12/E47, ZEB-1 and SIP-1) and shown to act through an interaction with proximal E-boxes of the E-cadherin promoter. We have analyzed the participation of another member of the Snail family, Slug, and observed that it also behaves as a repressor of E-cadherin expression. Stable expression of Slug in MDCK cells leads to the full repression of E-cadherin at transcriptional level and triggers a complete epithelial to mesenchymal transition. Slug-induced repression of E-cadherin is mediated by its binding to proximal E-boxes, particularly to the E-pal element of the mouse promoter. Detailed analysis of the binding affinity of different repressors to the E-pal element indicates that Slug binds with lower affinity than Snail and E47 proteins. These results, together with the known expression patterns of these factors in embryonic development and carcinoma cell lines, support the idea that the in vivo action of the different factors in E-cadherin repression can be modulated by their relative concentrations as well as by specific cellular or tumour contexts.
Key words: Slug, E-cadherin, Epithelial to mesenchymal transition (EMT)
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