1. ¹Institute of Pathology, University of Bonn, PO Box 2120, 53011 Bonn, Germany
2. ²CNRS UMR8526, Institut de Biologie de Lille, 1 rue Calmette, 59021 Lille Cedex, France

Correspondence: N Wernert, E-mail: nicolas.wernert@ukb.uni-bonn.de

³Current address: Institute of Neuropathology, Charité, Campus Virchow Klinikum, Humboldt University, Augustenbergerplatz 1, 13353 Berlin, Germany

Received 1 October 2004; Revised 3 March 2005; Accepted 18 April 2005; Published online 6 June 2005.

Abstract

Ets-1 is the prototype of the family of ETS transcription factors. In human tumors, Ets-1 is expressed in endothelial cells and fibroblasts of the tumor stroma and is proposed to play a role in tumor vascularization and invasion by upregulating expression of matrix-degrading proteases. In human carcinomas, Ets-1 is also expressed by neoplastic cells, but little is known about the functional implications of this observation. We have addressed the role of Ets-1 in epithelial HeLa tumor cells by selecting stably Ets-1 over and underexpressing HeLa cells. Ets-1 expression increases the transformed phenotype of HeLa cells, by promoting cell migration, invasion and anchorage-independent growth, while Ets-1 downregulation reduces cell attachment. In correlation with these results, Ets-1 upregulation increases integrin2 expression but not that of other integrins. These results suggest that, in addition to its role in the tumor stroma, Ets-1 may also promote tumor development and progression by increasing neoplastic transformation.