Targeting AMPK: a new therapeutic opportunity in breast cancer

Crit Rev Oncol Hematol. 2008 Jul;67(1):1-7. doi: 10.1016/j.critrevonc.2008.01.007. Epub 2008 Mar 14.

Abstract

Background: This paper reviews the mammalian Target Of Rapamycin (mTOR) pathway dysregulation in breast cancer, and the current evidence targeting this pathway directly or through activation of AMP-activated protein kinase (AMPK) as an additional therapeutic opportunity for intervention in breast cancer.

Methods: Relevant articles were identified through computerised searches of Medline and Pubmed. Secondary articles were identified from the reference lists of key papers and by hand searching.

Results and conclusion: The current consensus to target the AMPK/mTOR pathway in breast cancer is based on in vitro and epidemiological evidences. A low incidence of cancer in diabetic patients on metformin has been explained in vitro by the drug's anti-proliferative effect through activation of AMPK. There is a need to explore the anticancer effects of metformin and the potential to develop the therapeutic avenues offered by targeting the AMPK/mTOR pathway.

Publication types

  • Research Support, Non-U.S. Gov't
  • Review

MeSH terms

  • Animals
  • Breast Neoplasms / enzymology*
  • Female
  • Humans
  • Hypoglycemic Agents / pharmacology
  • Metformin / pharmacology
  • Protein Kinases / metabolism*
  • Signal Transduction / physiology*
  • TOR Serine-Threonine Kinases

Substances

  • Hypoglycemic Agents
  • Metformin
  • Protein Kinases
  • AMP-activated protein kinase kinase
  • MTOR protein, human
  • TOR Serine-Threonine Kinases