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 Blood, 29 October 2009, Vol. 114, No. 18, pp. 3890-3898.
Prepublished online as a Blood First Edition Paper on August 28, 2009; DOI 10.1182/blood-2009-01-201111.

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LYMPHOID NEOPLASIA

C/EBPβ regulates transcription factors critical for proliferation and survival of multiple myeloma cells

Rekha Pal1, Martin Janz2, Deborah L. Galson1, Margarete Gries2, Shirong Li1, Korinna Jöhrens3, Ioannis Anagnostopoulos3, Bernd Dörken2, Markus Y. Mapara1, Lisa Borghesi4, Lela Kardava4, G. David Roodman1, Christine Milcarek4, and Suzanne Lentzsch1

1 Division of Hematology/Oncology, University of Pittsburgh Cancer Institute, PA; 2 Hematology, Oncology, and Tumorimmunology, Max Delbrück Center for Molecular Medicine and Charité, University Medicine Berlin, Campus Virchow-Klinikum, Berlin, Germany; 3 Institute of Pathology, Charité University Medicine, Germany; and 4 Division of Immunology, University of Pittsburgh, PA

CCAAT/enhancer-binding protein β (C/EBPβ), also known as nuclear factor–interleukin-6 (NF-IL6), is a transcription factor that plays an important role in the regulation of growth and differentiation of myeloid and lymphoid cells. Mice deficient in C/EBPβ show impaired generation of B lymphocytes. We show that C/EBPβ regulates transcription factors critical for proliferation and survival in multiple myeloma. Multiple myeloma cell lines and primary multiple myeloma cells strongly expressed C/EBPβ, whereas normal B cells and plasma cells had little or no detectable levels of C/EBPβ. Silencing of C/EBPβ led to down-regulation of transcription factors such as IRF4, XBP1, and BLIMP1 accompanied by a strong inhibition of proliferation. Further, silencing of C/EBPβ led to a complete down-regulation of antiapoptotic B-cell lymphoma 2 (BCL2) expression. In chromatin immunoprecipitation assays, C/EBPβ directly bound to the promoter region of IRF4, BLIMP1, and BCL2. Our data indicate that C/EBPβ is involved in the regulatory network of transcription factors that are critical for plasma cell differentiation and survival. Targeting C/EBPβ may provide a novel therapeutic strategy in the treatment of multiple myeloma.


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