Current insights into the regulation of programmed cell death by NF-κB

J. Dutta, Y. Fan, N. Gupta, G. Fan, C. Gélinas

Research output: Contribution to journalReview articlepeer-review

351 Scopus citations

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.

Original languageEnglish (US)
Pages (from-to)6800-6816
Number of pages17
JournalOncogene
Volume25
Issue number51
DOIs
StatePublished - Oct 30 2006

All Science Journal Classification (ASJC) codes

  • Molecular Biology
  • Genetics
  • Cancer Research

Keywords

  • Apoptosis
  • Cancer
  • NF-kappaB
  • Necrosis
  • Transcription factor

Fingerprint

Dive into the research topics of 'Current insights into the regulation of programmed cell death by NF-κB'. Together they form a unique fingerprint.

Cite this