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Prepublished online as a Blood First Edition Paper on August 7, 2003; DOI 10.1182/blood-2003-03-0915.
Submitted March 25, 2003
Accepted July 23, 2003
JunB inhibits proliferation and transformation in B lymphoid cells
Agnieszka P Szremska, Lukas Kenner, Eva Weisz, Rene G Ott, Emmanuelle Passegue, Michaela Artwohl, Michael Freissmuth, Renate Stoxreiter, Hans-Christian Theussl, Sabina Baumgartner Parzer, Richard Moriggl, Erwin F Wagner, and Veronika Sexl*
Institute of Pharmacology, Vienna University, Vienna, Austria
Institute of Molecular Pathology, Vienna, Austria
Department of Endocrinology, University Clinics, Vienna, Austria
* Corresponding author; email: veronika.sexl{at}univie.ac.at.
The AP-1 member JunB has recently been implicated in leukemogenesis. Here we surveyed human lymphoma samples for expression of JunB and other AP-1 members (c-Jun, c-Fos, Fra1, JunD). JunB was strongly expressed in T cell lymphomas, but non-Hodgkin B cell lymphomas do not or only weakly express JunB. We therefore asked whether JunB acted as a negative regulator of B cell development, proliferation and transformation. We used transgenic mice that expressed JunB under the control of the Ubiquitin C promoter; these displayed increased JunB levels in both B and T lymphoid cells. JunB transgenic cells of B lymphoid, but not of T lymphoid origin responded poorly to mitogenic stimuli. Furthermore, JunB transgenic cells were found to be less susceptible to the transforming potential of the Abelson oncogene in vitro. In addition, overexpression of JunB partially protected transgenic mice against the oncogenic challenge in vivo. However, transformed B cells eventually escaped from the inhibitory effect of JunB: the proliferative response was similar in explanted tumor-derived cells from transgenic animals and those from wild type controls. Our results identify JunB as a novel regulator of B cell proliferation and transformation.
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