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Curr Mol Med. 2007 Nov;7(7):619-37.

Nuclear factor-kappa B: from clone to clinic.

Author information

1
Cytokine Research Laboratory, Department of Experimental Therapeutics, The University of Texas M. D. Anderson Cancer Center, Houston, TX 77030, USA.

Abstract

Nuclear transcription factor kappaB (NF-kappaB) was first discovered in 1986 in the nucleus of the B cell as an enhancer in the kappa immunoglobulin chain. However, this factor has identified in the cytoplasm in the resting state. When activated in response to inflammatory stimuli, carcinogens, stress, ionizing radiation, and growth factors; NF-kappaB translocates to the nucleus where it upregulates the expression of over 400 different gene products linked with inflammation, cell survival, proliferation, invasion, and angiogenesis. The activation of NF-kappaB has now been linked with a variety of inflammatory diseases, including cancer and pulmonary, autoimmune, skin, neurodegenerative, and cardiovascular disorders. Indeed, constitutive NF-kappaB activation frequently correlates with the proliferation, survival, chemoresistance, radioresistance, and progression of various cancers. Hence, NF-kappaB has both diagnostic and prognostic applications. In addition, pharmaceutical companies are aggressively pursuing development of inhibitors of NF-kappaB with therapeutic potential. Thus within last decades this transcription factor, discovered serendipitously, has moved from "clone to clinic".

PMID:
18045141
DOI:
10.2174/156652407782564363
[Indexed for MEDLINE]

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