KEAP1 E3 ligase-mediated downregulation of NF-kappaB signaling by targeting IKKbeta

Mol Cell. 2009 Oct 9;36(1):131-40. doi: 10.1016/j.molcel.2009.07.025.

Abstract

IkappaB kinase beta (IKKbeta) is involved in tumor development and progression through activation of the nuclear factor (NF)-kappaB pathway. However, the molecular mechanism that regulates IKKbeta degradation remains largely unknown. Here, we show that a Cullin 3 (CUL3)-based ubiquitin ligase, Kelch-like ECH-associated protein 1 (KEAP1), is responsible for IKKbeta ubiquitination. Depletion of KEAP1 led to the accumulation and stabilization of IKKbeta and to upregulation of NF-kappaB-derived tumor angiogenic factors. A systematic analysis of the CUL3, KEAP1, and RBX1 genomic loci revealed a high percentage of genome loss and missense mutations in human cancers that failed to facilitate IKKbeta degradation. Our results suggest that the dysregulation of KEAP1-mediated IKKbeta ubiquitination may contribute to tumorigenesis.

Publication types

  • Research Support, N.I.H., Extramural
  • Research Support, Non-U.S. Gov't
  • Research Support, U.S. Gov't, Non-P.H.S.

MeSH terms

  • Animals
  • Breast Neoplasms / genetics
  • Breast Neoplasms / metabolism
  • Carrier Proteins / genetics
  • Carrier Proteins / metabolism
  • Cell Line
  • Cell Line, Tumor
  • Cullin Proteins / genetics
  • Cullin Proteins / metabolism
  • DNA Copy Number Variations / genetics
  • Female
  • Gene Expression / drug effects
  • Gene Expression / genetics
  • Humans
  • I-kappa B Kinase / genetics
  • I-kappa B Kinase / metabolism*
  • Interleukin-8 / genetics
  • Intracellular Signaling Peptides and Proteins / physiology*
  • Kaplan-Meier Estimate
  • Kelch-Like ECH-Associated Protein 1
  • Mice
  • Mutation / physiology
  • NF-kappa B / metabolism*
  • Neoplasms / genetics
  • Neoplasms / metabolism
  • Neovascularization, Physiologic / genetics
  • Protein Binding / physiology
  • Protein Interaction Domains and Motifs / physiology
  • RNA, Small Interfering / genetics
  • Signal Transduction / drug effects
  • Signal Transduction / physiology*
  • Transcription Factor RelA / metabolism
  • Transfection
  • Tumor Necrosis Factor-alpha / pharmacology
  • Ubiquitination / physiology

Substances

  • CUL3 protein, human
  • Carrier Proteins
  • Cullin Proteins
  • Interleukin-8
  • Intracellular Signaling Peptides and Proteins
  • KEAP1 protein, human
  • Kelch-Like ECH-Associated Protein 1
  • NF-kappa B
  • RBX1 protein, human
  • RELA protein, human
  • RNA, Small Interfering
  • Transcription Factor RelA
  • Tumor Necrosis Factor-alpha
  • I-kappa B Kinase