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J. Biol. Chem., Vol. 280, Issue 2, 887-898, January 14, 2005

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Pea3 Transcription Factor Cooperates with USF-1 in Regulation of the Murine bax Transcription without Binding to an Ets-binding Site^*

Virginie Firlej¶, Béatrice Bocquet, Xavier Desbiens, Yvan de Launoit||, and Anne Chotteau-Lelièvre**

From the Laboratoire de Biologie du Développement UPRES-EA1033, Université des Sciences et Technologies de Lille, 59655 Villeneuve d'Ascq Cedex, Régulation Transcriptionnelle au Cours de la Tumorigenèse Mammaire, UMR 8117/CNRS/USTL, Institut Pasteur de Lille/Institut de Biologie de Lille, 1 Rue Calmette, 59021 Lille Cedex, France, and ^||Laboratoire de Virologie Moléculaire, Faculté de Médecine, ULB, CP 614, 808 Route de Lennik, 1070 Brussels, Belgium

The Pea3 transcription factor (which belongs to the PEA3 group) from the Ets family has been shown to be involved in mammary embryogenesis and oncogenesis. However, except for proteinases, only few of its target genes have been reported. In the present report, we identified bax as a Pea3 up-regulated gene. We provide evidence of this regulation by using Pea3 overexpression and Pea3 silencing in a mammary cell line. Both Pea3 and Erm, another member of the PEA3 group, are able to transactivate bax promoter fragments. Although the minimal Pea3-regulated bax promoter does not contain an Ets-binding site, two functional upstream stimulatory factor-regulated E boxes are present. We further demonstrate the ability of Pea3 and USF-1 to cooperate for the transactivation of the bax promoter, mutation of the E boxes dramatically reducing the Pea3 transactivation potential. Although Pea3 did not directly bind to the minimal bax promoter, we provide evidence that USF-1 could form a ternary complex with Pea3 and DNA. Taken together, our results suggest that Pea3 may regulate bax transcription via the interaction with USF-1 but without binding to DNA.

Received for publication, July 15, 2004 , and in revised form, September 30, 2004.

^* This work was supported in part by the Ligue Nationale Contre le Cancer, the Association pour la Recherche sur le Cancer, the Institut Pasteur de Lille, the CNRS, the Fonds National de la Recherche Scientifique, Belgium, and the Université des Sciences et Technologies de Lille. The costs of publication of this article were defrayed in part by the payment of page charges. This article must therefore be hereby marked "advertisement" in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.

^¶ Supported by the Ligue Nationale Contre le Cancer.

^** To whom correspondence should be addressed. Tel.: 33-320-87-11-28; Fax: 33-320-87-11-11; E-mail: anne.chotteau{at}ibl.fr.

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