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 Blood, 15 March 2007, Vol. 109, No. 6, pp. 2597-2603.
Prepublished online as a Blood First Edition Paper on December 5, 2006; DOI 10.1182/blood-2006-05-020545.

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NEOPLASIA

Bmi-1 is induced by the Epstein-Barr virus oncogene LMP1 and regulates the expression of viral target genes in Hodgkin lymphoma cells

Amanda Dutton1, Ciaran B. Woodman1, Marilyn B. Chukwuma1, James I. K. Last1, Wenbin Wei1, Martina Vockerodt1, Karl R. N. Baumforth1, Joanne R. Flavell1, Martin Rowe1, A. Malcolm R. Taylor1, Lawrence S. Young1, and Paul G. Murray1

1 Cancer Research UK Institute for Cancer Studies, The Medical School, University of Birmingham, Edgbaston, United Kingdom

Polycomb group (PcG) proteins are chromatin modifiers that are necessary for the maintenance and renewal of embryonic and adult stem cells. However, overexpression of the PcG protein, Bmi-1, causes lymphoma in transgenic mice. We show that Bmi-1 is up-regulated in Hodgkin lymphoma (HL) cells by the Epstein-Barr virus (EBV) oncogene latent membrane protein-1 (LMP1) and that this up-regulation is mediated by NF-{kappa}B signaling. We also show that Bmi-1 is up-regulated by NF-{kappa}B in EBV-negative HL cells. Down-regulation of LMP1 and Bmi-1 decreased the survival of HL cells, suggesting that Bmi-1 may mediate the prosurvival effects of LMP1-induced NF-{kappa}B signaling in HL cells. Transcriptional targets of Bmi-1 were identified after its knockdown in an HL cell line. We show here that Bmi-1 and LMP1 down-regulate the ataxia telangiectasia–mutated (ATM) tumor suppressor and conclude that Bmi-1 contributes to LMP1-induced oncogenesis in HL.


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