Terpestacin inhibits tumor angiogenesis by targeting UQCRB of mitochondrial complex III and suppressing hypoxia-induced reactive oxygen species production and cellular oxygen sensing

J Biol Chem. 2010 Apr 9;285(15):11584-95. doi: 10.1074/jbc.M109.087809. Epub 2010 Feb 9.

Abstract

Cellular oxygen sensing is required for hypoxia-inducible factor-1alpha stabilization, which is important for tumor cell survival, proliferation, and angiogenesis. Here we find that terpestacin, a small molecule previously identified in a screen of microbial extracts, binds to the 13.4-kDa subunit (UQCRB) of mitochondrial Complex III, resulting in inhibition of hypoxia-induced reactive oxygen species generation. Consequently, such inhibition blocks hypoxia-inducible factor activation and tumor angiogenesis in vivo, without inhibiting mitochondrial respiration. Overexpression of UQCRB or its suppression using RNA interference demonstrates that it plays a crucial role in the oxygen sensing mechanism that regulates responses to hypoxia. These findings provide a novel molecular basis of terpestacin targeting UQCRB of Complex III in selective suppression of tumor progression.

Publication types

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

MeSH terms

  • Animals
  • Bridged Bicyclo Compounds / pharmacology
  • Carrier Proteins / metabolism*
  • Electron Transport Complex III / metabolism*
  • Endothelium, Vascular / cytology
  • Female
  • Hypoxia*
  • Mice
  • Mice, Inbred C3H
  • Mitochondria / metabolism*
  • Neoplasm Transplantation
  • Neovascularization, Pathologic*
  • Oxygen / metabolism*
  • Reactive Oxygen Species*
  • Vascular Endothelial Growth Factor A / metabolism

Substances

  • Bridged Bicyclo Compounds
  • Carrier Proteins
  • Reactive Oxygen Species
  • Vascular Endothelial Growth Factor A
  • ubiquinone-binding proteins
  • terpestacin
  • Electron Transport Complex III
  • Oxygen