Nuclear factor-κB, p53, and mitochondria: regulation of cellular metabolism and the Warburg effect

Trends Biochem Sci. 2012 Aug;37(8):317-24. doi: 10.1016/j.tibs.2012.04.002. Epub 2012 May 23.


Among the characteristics acquired by many tumour cells is a shift from using oxidative phosphorylation to using glycolysis for ATP production. Although the nuclear factor (NF)-κB family of transcriptional regulators have important roles in tumorigenesis, their ability to function as regulators of metabolism has only been recently investigated. This has revealed the importance of crosstalk between NF-κB, the p53 tumour suppressor and other crucial cell signalling pathways. This review discusses the mechanisms through which NF-κB regulates tumour cell metabolism and the important role of p53 in determining the consequences of NF-κB activity. It also proposes a model in which NF-κB contributes to the shift to glycolytic ATP production through regulation of both nuclear and mitochondrial gene expression.

Publication types

  • Research Support, Non-U.S. Gov't
  • Review

MeSH terms

  • Adenosine Triphosphate / metabolism
  • Animals
  • Cell Nucleus / genetics
  • Cell Nucleus / metabolism
  • Cell Transformation, Neoplastic / genetics
  • Cell Transformation, Neoplastic / metabolism*
  • Gene Expression Regulation, Neoplastic*
  • Glycolysis
  • Humans
  • Hypoxia-Inducible Factor 1 / genetics
  • Hypoxia-Inducible Factor 1 / metabolism
  • Mitochondria / genetics
  • Mitochondria / metabolism*
  • NF-kappa B / genetics
  • NF-kappa B / metabolism*
  • Oxidative Phosphorylation
  • Protein Transport
  • Transcription Factors / genetics
  • Transcription Factors / metabolism
  • Transcription, Genetic
  • Tumor Suppressor Protein p53 / genetics
  • Tumor Suppressor Protein p53 / metabolism*


  • Hypoxia-Inducible Factor 1
  • NF-kappa B
  • Transcription Factors
  • Tumor Suppressor Protein p53
  • Adenosine Triphosphate