Metabolic regulation by SIRT3: implications for tumorigenesis

Trends Mol Med. 2012 Sep;18(9):516-23. doi: 10.1016/j.molmed.2012.05.004. Epub 2012 Jun 27.

Abstract

Cancer cells meet their needs for energy and biomass production by consuming high levels of nutrients and rewiring metabolism to support macromolecular biosynthesis. Mitochondrial enzymes play central roles in anabolic growth, and acetylation may provide a key layer of regulation over mitochondrial metabolic pathways. As a major mitochondrial deacetylase, SIRT3 regulates the activity of enzymes to coordinate global shifts in cellular metabolism. SIRT3 promotes the function of the tricarboxylic acid (TCA) cycle and the electron transport chain and reduces oxidative stress. Loss of SIRT3 triggers oxidative damage, reactive oxygen species (ROS)-mediated signaling, and metabolic reprogramming to support proliferation and tumorigenesis. Thus, SIRT3 is an intriguing example of how nutrient-sensitive, post-translational regulation may provide integrated regulation of metabolic pathways to promote metabolic homeostasis in response to diverse nutrient signals.

Publication types

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

MeSH terms

  • Acetylation
  • Animals
  • Cell Transformation, Neoplastic*
  • Citric Acid Cycle
  • Humans
  • Oxidative Stress
  • Protein Processing, Post-Translational
  • Reactive Oxygen Species / metabolism
  • Sirtuin 3 / genetics
  • Sirtuin 3 / metabolism*

Substances

  • Reactive Oxygen Species
  • SIRT3 protein, human
  • Sirtuin 3