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Originally published In Press as doi:10.1074/jbc.M011224200 on April 25, 2001

J. Biol. Chem., Vol. 276, Issue 27, 24661-24666, July 6, 2001
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Loss of E-cadherin Expression in Melanoma Cells Involves Up-regulation of the Transcriptional Repressor Snail*

Ina PoserDagger , David Domínguez§, Antonio Garcia de Herreros§, Alinda VarnaiDagger , Reinhard BuettnerDagger , and Anja K BosserhoffDagger

From the Dagger  Institute of Pathology, Medical School Rheinisch-Westfälische Technische Hochschule (RWTH) Aachen, D-52074 Aachen, Germany and § Unitat de Biologia Cellular i Molecular, Institut Municipal d'Investigacio Medica, Universitat Pompeu Fabra, 08003 Barcelona, Spain

Malignant transformation of melanocytes frequently coincides with loss of E-cadherin expression. Here we show that loss of E-cadherin in melanoma cell lines does not involve mutations in the E-cadherin gene, promoter methylation, or alterations in expression of AP-2 transcription factors as suggested previously. In a panel of different melanoma cell lines, E-cadherin expression was negatively regulated by up-regulation of the transcription factor Snail. In comparison with primary human melanocytes, where Snail expression was not detected by reverse transcription-polymerase chain reaction, significant expression was found in all eight melanoma cell lines. In parallel, Western blot and reverse transcription-polymerase chain reaction analysis revealed strong reduction of E-cadherin expression in the melanoma cells. Consistently, transient transfection of a Snail expression plasmid into human primary melanocytes led to significant down-regulation of E-cadherin, whereas transient and stable transfection of an antisense Snail construct induced reexpression of E-cadherin in Mel Ju and Mel Im melanomas. In summary, we conclude that activation of Snail expression plays an important role in down-regulation of E-cadherin and tumorigenesis of malignant melanomas.

* This work was supported by grants from the Deutsche Forschungsgemeinschaft and the Deutsche Krebshilfe (to A. K. B. and R. B.) and by Grant PM 99-0132 from the Ministerio de Ciencia y Tecnologia (to A. G. d. H.).The costs of publication of this article were defrayed in part by the payment of page charges. The article must therefore be hereby marked "advertisement" in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.

To whom correspondence should be addressed: Institute of Pathology, Medical School Rheinisch-Westfälische Technische Hochschule (RWTH) Aachen, Pauwelsstrasse 30, D-52074 Aachen, Germany. Tel.: 49-241-8088080; Fax: 49-241-8888439; E-mail: bosserhoff@pat.rwth- aachen.de.

Copyright © 2001 by The American Society for Biochemistry and Molecular Biology, Inc.


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