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Oncogenes, tumor suppressors and p52 NF-κB

Oncogene volume 22, pages 7553–7556 (2003)Cite this article

Abstract

A role for the p52 NF-κB subunit in tumorigenesis has been steadily emerging since its discovery as a gene associated with chromosomal translocations in B- and T-cell lymphomas. Now Eliopoulos and co-workers have extended these studies to examine the effect of the Epstein–Barr virus (EBV)-encoded latent infection membrane protein 1 (LMP1) on p52. They find that LMP1 stimulates the processing of p100 to p52 NF-κB. Moreover, nuclear p52 is also associated with LMP1 expression in tumor tissue biopsies. They also demonstrate that the pathway leading to p100/p52 processing is distinct from that engaged by LMP1 to activate other NF-κB subunits through IκBα degradation. A clearer picture is now developing of the important role that p52 NF-κB plays during normal cell growth and how subverting its function can contribute to oncogenesis.

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Acknowledgements

NDP is the recipient of a Royal Society University Research Fellowship.

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  1. Division of Gene Regulation and Expression, School of Life Sciences, MSI/WTB Complex, Dow Street, University of Dundee, Dundee, DD1 5EH, UK

    Neil D Perkins

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  1. Neil D Perkins
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Correspondence to Neil D Perkins.

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Commentary article on Eliopoulos et al. ‘Epstein–Barr virus-encoded latent infection membrane protein 1 (LMP1) regulates the processing of p100 NF-κB to p52 via an IKKγ/NEMO-independent signaling pathway’

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Perkins, N. Oncogenes, tumor suppressors and p52 NF-κB. Oncogene 22, 7553–7556 (2003). https://doi.org/10.1038/sj.onc.1207139

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