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Glycolysis links p53 function with NF‐κB signaling: Impact on cancer and aging process
Author(s) -
Salminen Antero,
Kaarniranta Kai
Publication year - 2010
Publication title -
journal of cellular physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.529
H-Index - 174
eISSN - 1097-4652
pISSN - 0021-9541
DOI - 10.1002/jcp.22119
Subject(s) - glycolysis , warburg effect , anaerobic glycolysis , microbiology and biotechnology , oxidative phosphorylation , oncogene , biology , signal transduction , cancer , chemistry , biochemistry , cancer research , metabolism , apoptosis , cell cycle , genetics
In 1930, Otto Warburg observed that cancer cells produce an increased amount of their energy through aerobic glycolysis and subsequently, this was called the Warburg effect. During aging, the capacity for mitochondrial respiration clearly declines and aerobic glycolysis appears to compensate for the deficiency in oxidative metabolism. This shift in energy production, both in aging and cancer, could protect from the toxic effects of oxygen free radicals whereas increased glycolysis can have adverse effects. It was recently demonstrated that the glycolysis‐linked protein O ‐glycosylation can potentiate the catalytic activity of IKKβ and subsequently trigger NF‐κB signaling. It seems that tumor suppressor oncogene p53 has an important role in the regulation of protein O ‐glycosylation since p53 is a potent inhibitor of glycolysis, for example, via TIGAR protein expression. Aging is known to repress the function of p53 and this could enhance glycolysis and NF‐κB signaling. We will discuss the role of p53 in the regulation of glycolysis‐dependent activation of NF‐κB signaling in both cancer and aging process. J. Cell. Physiol. 224:1–6, 2010 © 2010 Wiley‐Liss, Inc.