NF-κB: Regulation by Methylation

Cancer Research
Tao Lu, George R Stark

Abstract

In normal cells exposed to stress, the central transcription factor NF-κB is activated only transiently, to modulate the activation of downstream immune responses. However, in most cancers, NF-κB is abnormally activated constitutively, contributing thus to oncogenesis and tumor progression. Therefore, downregulating NF-κB activity is an important goal of cancer treatment. In order to control NF-κB activity therapeutically, it is helpful to understand the molecular mechanisms that normally govern its activation and how dysregulated NF-κB activity may aid the development of disease. Recent evidence from our laboratories and others indicates that, in addition to various posttranslational modifications of NF-κB that have been observed previously, including phosphorylation, ubiquitination, and acetylation, NF-κB can be methylated reversibly on lysine or arginine residues by histone-modifying enzymes, including lysine and arginine methyl transferases and demethylases. Furthermore, these methylations are required to activate many downstream genes. Interestingly, amplifications and mutations of several such enzymes have been linked to cancer. We propose that some of these mutations may alter the methylation not only of histones but als...Continue Reading

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Citations

Mar 19, 2016·Wiley Interdisciplinary Reviews. Systems Biology and Medicine·Simon MitchellAlexander Hoffmann
Jan 9, 2017·Food and Chemical Toxicology : an International Journal Published for the British Industrial Biological Research Association·Zhi-Jing HeKai Wang
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Dec 7, 2021·Frontiers in Cardiovascular Medicine·Rosaria Anna FontanellaMichelangela Barbieri

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