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Keratoepithelin Suppresses the Progression of Experimental Human Neuroblastomas

¹ Abteilung Pädiatrie I, Zentrum Kinderheilkunde und Jugendmedizin, Klinikum der Georg-August-Universität Göttingen, Göttingen, Germany; ² Abteilung Hämatologie, Onkologie und Endokrinologie, Universitätsklinikum Essen-Duisburg, Essen, Germany; ³ Institut für Biochemie II und Zentrum für Molekulare Medizin Köln, Universität zu Köln, Köln, Germany; and ⁴ Institut de Recherche en Ophtalmologie, Department of Ophthalmology, University of Lausanne, Sion, Switzerland

Requests for reprints: Lothar Schweigerer, Abteilung Pädiatrie I, Zentrum Kinderheilkunde und Jugendmedizin, Klinikum der Georg-August-Universität Göttingen, D-37075 Göttingen, Germany. Phone: 49-551-39-6200; Fax: 49-551-39-6231; E-mail: Lothar.Schweigerer{at}med.uni-goettingen.de.

Neuroblastoma is the most common extracranial childhood tumor. High expression of activin A is associated with a favorable prognosis, but the contributing mechanisms have remained unclear. Our previous demonstration of the activin A–mediated up-regulation of keratoepithelin led to the consideration that keratoepithelin could modulate neuroblastoma growth and/or progression. We report here that enhanced keratoepithelin expression in human neuroblastoma cells suppresses neuroblastoma cell cohesion and adhesion to various extracellular matrix proteins and that it inhibits neuroblastoma cell proliferation and invasion in vitro and in vivo. Using microarray analysis, we identified several keratoepithelin-regulated genes that may contribute to these biological changes. Together with the observation that keratoepithelin is expressed in human neuroblastomas in vivo, our data suggest that keratoepithelin could play a beneficial role in neuroblastoma development and/or progression. (Cancer Res 2006; 66(10): 5314-21)

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