Abstract
The nuclear factor-kappaB (NF-κB) transcription factors have emerged as major regulators of programmed cell death (PCD) whether via apoptosis or necrosis. In this context, NF-κB's activity has important ramifications for normal tissue development, homoeostasis and the physiological functions of various cell systems including the immune, hepatic, epidermal and nervous systems. However, improper regulation of PCD by NF-κB can have severe pathologic consequences, ranging from neurodegeneration to cancer, where its activity often precludes effective therapy. Although NF-κB generally protects cells by inducing the expression genes encoding antiapoptotic and antioxidizing proteins, its role in apoptosis and necrosis can vary markedly in different cell contexts, and NF-κB can sensitize cells to death-inducing stimuli in some instances. This article describes our current knowledge of the role of NF-κB in apoptosis and necrosis, and focuses on the many advances since we last reviewed this rapidly evolving topic in Oncogene 3 years ago. There has been substantial progress in understanding NF-κB's mode of action in apoptosis and necrosis and the mechanisms that regulate its anti- vs proapoptotic activities. These recent developments shed new light on the role of NF-κB in many disease conditions including tumor development, tumor progression and anticancer treatment.
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Acknowledgements
We regret our inability to mention the work of many investigators due to space restrictions. Research in this laboratory on the roles of NF-κB in PCD and cancer, and on NF-κB's antiapoptotic target Bfl-1/A1 is supported by grants from the National Institutes of Health CA54999 and CA83937 and from the New Jersey Commission on Cancer Research to CG.
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Dutta, J., Fan, Y., Gupta, N. et al. Current insights into the regulation of programmed cell death by NF-κB. Oncogene 25, 6800–6816 (2006). https://doi.org/10.1038/sj.onc.1209938
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DOI: https://doi.org/10.1038/sj.onc.1209938
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