Regulation of mammalian target of rapamycin complex 1 (mTORC1) by hypoxia: causes and consequences

Target Oncol. 2011 Jun;6(2):95-102. doi: 10.1007/s11523-011-0173-x. Epub 2011 Apr 16.

Abstract

Integration of cellular and extracellular signals maintains tissue homeostasis under conditions of normal proliferation and stress. A central player in regulating responses to stress is the serine/threonine kinase mammalian target of rapamycin (mTOR). In many cancers, mTOR complex 1 (mTORC1) signaling is enhanced, even under conditions where such signaling should be suppressed. This article reviews some of the details that are emerging on how low oxygen (hypoxia) regulates mTORC1 signaling, and the consequences for dysregulation in pediatric solid tumors.

Publication types

  • Review

MeSH terms

  • Ataxia Telangiectasia Mutated Proteins
  • Cell Cycle Proteins / metabolism
  • Cell Hypoxia / physiology
  • Child
  • DNA-Binding Proteins / metabolism
  • Humans
  • Mechanistic Target of Rapamycin Complex 1
  • Multiprotein Complexes
  • Neoplasms / metabolism*
  • Neoplasms / pathology
  • Protein-Serine-Threonine Kinases / metabolism
  • Proteins / metabolism*
  • Signal Transduction
  • TOR Serine-Threonine Kinases
  • Tumor Suppressor Proteins / metabolism

Substances

  • Cell Cycle Proteins
  • DNA-Binding Proteins
  • Multiprotein Complexes
  • Proteins
  • Tumor Suppressor Proteins
  • TOR Serine-Threonine Kinases
  • ATM protein, human
  • Ataxia Telangiectasia Mutated Proteins
  • Mechanistic Target of Rapamycin Complex 1
  • Protein-Serine-Threonine Kinases