Targeting AMPK: a new therapeutic opportunity in breast cancer.
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.


CONCLUSIONS
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.
Hadad
Sirwan M
SM
Department of Surgery and Molecular Oncology, Ninewells Hospital and Medical School, Dundee, Scotland, United Kingdom. s.hadad@dundee.ac.uk
Fleming
Stewart
S
Thompson
Alastair M
AM
D000091162:AMP-Activated Protein Kinase Kinases; D000818:Animals; D001943:Breast Neoplasms / Q000201:enzymology*; D005260:Female; D006801:Humans; D007004:Hypoglycemic Agents / Q000494:pharmacology; D008687:Metformin / Q000494:pharmacology; D011494:Protein Kinases / Q000378:metabolism*; D015398:Signal Transduction / Q000502:physiology*; D058570:TOR Serine-Threonine Kinases
D007004:Hypoglycemic Agents; D008687:Metformin; D011494:Protein Kinases; C546842:MTOR protein, human; D058570:TOR Serine-Threonine Kinases; D000091162:AMP-Activated Protein Kinase Kinases