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J. Biol. Chem., Vol. 278, Issue 30, 27988-27996, July 25, 2003

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YB-1 as a Cell Cycle-regulated Transcription Factor Facilitating Cyclin A and Cyclin B1 Gene Expression^*

Karsten Jürchott   ¶, Stephan Bergmann  ||, Ulrike Stein , Wolfgang Walther , Martin Janz **, Isabella Manni , Giulia Piaggio , Ellen Fietze , Manfred Dietel  and Hans-Dieter Royer 

From the Max-Delbrück-Centrum für Molekulare Medizin, Robert-Rössle-Strasse 10, 13092 Berlin, Germany, the Humboldt-Universität zu Berlin, Universitätsklinikum Charité, Institut für Pathologie, Schumannstrasse 20-21, 10117 Berlin, Germany, the ^**Humboldt-Universität zu Berlin, Universitätsklinikum Charité, Robert-Rössle-Klinik, Lindenberger Weg 80, 13125 Berlin, Germany, the Center of Advanced European Studies and Research (caesar), Ludwig-Erhard-Allee 2, 53175 Bonn, Germany, the ^||Institut für Humangenetik und Anthroplogie, Postfach 101001, 40001 Düsseldorf, Germany, and the Laboratorio di Oncogenesi Molecolare, Istituto Regina Elena, Via delle Messi D'Oro 156, 00158 Rome, Italy

Expression of the Y-box protein YB-1 is increased in proliferating normal and cancer cells, but its role in cell proliferation and cell cycle progression is unclear. We have identified a cell cycle-dependent relocalization of YB-1 from the cytoplasm to the nucleus at the G₁/S phase transition and demonstrate that both the charged zipper and the cold shock domain are involved in regulating this process. Using cell lines that constitutively overexpress YB-1, we show that nuclear accumulation of YB-1 is associated with increased cyclin A and cyclin B1 mRNA and protein expression. We provide evidence that deregulated YB-1 expression is linked to adhesion-independent cell proliferation through the induction of cyclin A. Thus, we have identified YB-1 as a cell cycle stage-specific transcription factor important for cell proliferation.

Received for publication, December 19, 2002 , and in revised form, April 7, 2003.

^* This work was supported by the Berliner Krebsgesellschaft (Interdisciplinary Research Project in Molecular Biology and Clinic of Breast and Ovarian Cancers). This work was partially supported by Grant ICS-120.4/RA00-90 from AIRC and grants from Ministero della Sanita. 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.

^¶ To whom correspondence should be addressed: Universitätsklinikum Charité, Institut für Pathologie, Schumannstrasse 20-21, D-10117 Berlin, Germany. Tel.: 49-30-450-536-194; Fax: 49-30-450-536-909; E-mail: karsten.juerchott{at}charite.de.

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