Hypoxia-induced pathways in breast cancer

Microsc Res Tech. 2002 Oct 1;59(1):41-8. doi: 10.1002/jemt.10175.

Abstract

Hypoxia, a common consequence of solid tumor growth in breast cancer and other cancers, serves to propagate a cascade of molecular pathways which include angiogenesis, glycolysis, and alterations in microenvironmental pH. Hypoxia-inducible factors, heterodimeric DNA binding complexes composed of two subunits, provide critical regulation of this response. This review presents a synopsis of the genes induced by hypoxia in the context of breast cancer and discusses how upregulation of HIF-1 activity, and the homologous factor HIF-2, are not only fundamental for the adaptation to hypoxia but also may be critical for tumor progression.

Publication types

  • Review

MeSH terms

  • Basic Helix-Loop-Helix Transcription Factors
  • Breast Neoplasms / physiopathology*
  • Carbonic Anhydrases / genetics
  • Carbonic Anhydrases / metabolism
  • Cell Hypoxia*
  • DNA-Binding Proteins / genetics
  • DNA-Binding Proteins / metabolism*
  • Female
  • Gene Expression Regulation, Neoplastic*
  • Glycolysis
  • Humans
  • Hypoxia-Inducible Factor 1
  • Hypoxia-Inducible Factor 1, alpha Subunit
  • Neoplasm Proteins / genetics
  • Neoplasm Proteins / metabolism
  • Neovascularization, Pathologic
  • Nuclear Proteins / genetics
  • Nuclear Proteins / metabolism*
  • Peptide Initiation Factors / genetics
  • Peptide Initiation Factors / metabolism*
  • Transcription Factors*

Substances

  • Basic Helix-Loop-Helix Transcription Factors
  • DNA-Binding Proteins
  • HIF1A protein, human
  • Hypoxia-Inducible Factor 1
  • Hypoxia-Inducible Factor 1, alpha Subunit
  • Neoplasm Proteins
  • Nuclear Proteins
  • Peptide Initiation Factors
  • Transcription Factors
  • endothelial PAS domain-containing protein 1
  • Carbonic Anhydrases