Leptin, estrogens and cancer

Mini Rev Med Chem. 2006 Aug;6(8):897-907. doi: 10.2174/138955706777934973.

Abstract

Obesity is a state of leptin resistance in which the membrane leptin receptor and the JAK-STAT pathway are blocked. This leads to increased intracellular concentrations of lipid metabolites, increased non-oxidative metabolism by adipocytes, and stimulation of the cell estrogen cycle. These factors are potentially oncogenic via the shared mitogen-activated protein kinase (MAPK), mitogen/extracellular signal-regulated kinase (MEK) and extracellular signal-regulated kinase (ERK) cellular pathways.

Publication types

  • Review

MeSH terms

  • Adipocytes / metabolism
  • Animals
  • Enzyme Inhibitors / pharmacology
  • Estrogens / metabolism*
  • Extracellular Signal-Regulated MAP Kinases / antagonists & inhibitors
  • Extracellular Signal-Regulated MAP Kinases / metabolism
  • Humans
  • Leptin / metabolism*
  • Lipids / blood
  • MAP Kinase Kinase Kinases / antagonists & inhibitors
  • MAP Kinase Kinase Kinases / metabolism
  • Mitogen-Activated Protein Kinase Kinases / antagonists & inhibitors
  • Mitogen-Activated Protein Kinase Kinases / metabolism
  • Neoplasms / enzymology
  • Neoplasms / metabolism*
  • Obesity / enzymology
  • Obesity / metabolism*
  • Obesity / pathology
  • Protein-Tyrosine Kinases / metabolism
  • Receptors, Cell Surface / metabolism
  • Receptors, Estrogen / metabolism
  • Receptors, Leptin
  • STAT Transcription Factors / metabolism

Substances

  • Enzyme Inhibitors
  • Estrogens
  • LEPR protein, human
  • Leptin
  • Lipids
  • Receptors, Cell Surface
  • Receptors, Estrogen
  • Receptors, Leptin
  • STAT Transcription Factors
  • Protein-Tyrosine Kinases
  • Extracellular Signal-Regulated MAP Kinases
  • MAP Kinase Kinase Kinases
  • Mitogen-Activated Protein Kinase Kinases