The NF-κB transcription factor is ubiquitously expressed and controls the expression of a large number of genes. Experimental data clearly indicate that NF-κB is a major regulator of the inflammatory reaction by controlling the expression of pro-inflammatory molecules in response to cytokines, oxidative stress and infectious agents. We demonstrated that NF-κB activation by IL-1β follows three distinct cell-specific pathways. Moreover, our studies indicated that in one model of inflammatory diseases, horse recurrent airway obstruction (RAO), the extent of NF-κB basal activity correlates with pulmonary dysfunction. Another role of NF-κB activity protects cancer cells against apoptosis and could participate in the resistance to cancer treatment. However, we did not observe any increased cytotoxicity after treatment with anticancer drugs or TNF-α of cells expressing a NF-κB inhibitor. Therefore, we can conclude that the inhibition of apoptosis by NF-κB is likely to be cell type and stimulus-dependent. Further studies are required to determine whether NF-κB could be a target for anticancer treatments. (C) 2000 Elsevier Science Ireland Ltd.
- Transcription factors
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