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Tumorigenesis

Inflammatory debate

Nature Reviews Cancer volume 4, page 753 (2004)Cite this article

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Patients with the inflammatory bowel disease ulcerative colitis are treated with non-steroidal anti-inflammatory drugs (NSAIDs) to reduce both disease symptoms and the increased risk of colitis-associated cancer (CAC). Michael Karin and colleagues investigated the activation of NF-κB in a mouse model of CAC. NSAIDs reportedly inhibit the function of an NF-κB activator, IKKβ. So, Karin and colleagues used mice with tissue-specific deletion of IKKβ to inhibit NF-κB activation

To induce colonic tumours in these mice, the authors used a pro-carcinogen — azoxymethane — and three doses of the pro-inflammatory sodium salt dextran sulphate. Mice lacking IKKβ in their intestinal epithelial cells had a markedly reduced occurrence of tumours compared with controls, indicating that NF-κB is important for tumour initiation and/or promotion. What might be the underlying mechanism for this? The inflammatory response, which induced apoptosis in the epithelial cells, was more severe in mice with IKKβ-deficient epithelial cells and was highlighted by the increased incidence of apoptosis in these cells. As NF-κB is a potent anti-apoptotic transcription factor, the authors concluded that the decreased rate of tumour incidence in these mice is due to increased apoptosis resulting from a lack of active NF-κB.

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ORIGINAL RESEARCH PAPER

  1. Greten, F. R. et al. IKKβ links inflammation and tumorigenesis in a mouse model of colitis-associated cancer. Cell 118, 285–296 (2004)

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  2. Pikarsky, E. et al. NF-κB functions as a tumour promoter in inflammation-associated cancer. Nature 25 Aug 2004 (doi:10.1038/nature02924)

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Authors
  1. Nicola McCarthy
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McCarthy, N. Inflammatory debate. Nat Rev Cancer 4, 753 (2004). https://doi.org/10.1038/nrc1461

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  • DOI: https://doi.org/10.1038/nrc1461

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