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J. Biol. Chem., Vol. 280, Issue 32, 29186-29193, August 12, 2005

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The Calcium-binding Protein S100A2 Interacts with p53 and Modulates Its Transcriptional Activity^*

Andrea Mueller, Beat W. Schäfer¶, Stefano Ferrari¶||, Mirjam Weibel, Miro Makek**, Matthias Höchli, and Claus W. Heizmann

From the Division of Clinical Chemistry and Biochemistry, Department of Pediatrics, Steinwiesstrasse 75, 8032 Zurich, the Division of Oncology, Department of Pediatrics, Steinwiesstrasse 75, 8032 Zurich, the ^||Institute of Molecular Cancer Research, University of Zurich, Winterthurerstrasse 190, 8057 Zurich, the ^**Pathologie-Institut für Bioptische Diagnostik, Forchstrasse 291, 8029 Zurich, and the Center of Microscopy of the University of Zurich, Gloriastrasse 30/32, 8006 Zurich, Switzerland

Head and neck squamous cell carcinoma express high levels of the EF-hand calcium-binding protein S100A2 in contrast to other tumorigenic tissues and cell lines where the expression of this protein is reduced. Subtractive hybridization of tumorigenic versus normal tumor-derived mammary epithelial cells has previously identified the S100A2 protein as potential tumor suppressor. The biological function of S100A2 in carcinogenesis, however, has not been elucidated to date. Here, we report for the first time that during recovery from hydroxyurea treatment, the S100A2 protein translocated from the cytoplasm to the nucleus and co-localized with the tumor suppressor p53 in two different oral carcinoma cells (FADU and SCC-25). Co-immunoprecipitation experiments and electrophoretic mobility shift assay showed that the interaction between S100A2 and p53 is Ca²⁺-dependent. Preliminary characterization of this interaction indicated that the region in p53 involved with binding to S100A2 is located at the C terminus of p53. Finally, luciferase-coupled transactivation assays, where a p53-reporter construct was used, indicated that interaction with S100A2 increased p53 transcriptional activity. Our data suggest that in oral cancer cells the Ca²⁺- and cell cycle-dependent p53-S100A2 interaction might modulate proliferation.

Received for publication, May 6, 2005

^* This work was supported by the Julius-Müller Stiftung and Förderung des Akademischen Nachwuchses of the University of Zürich, Switzerland. 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.

^¶ Both authors contributed equally to this work.

To whom correspondence should be addressed. Tel.: 41-44-266-7541; Fax: 41-44-266-71-69; E-mail: claus.heizmann{at}kispi.unizh.ch.

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