Metformin Treatment for the Prevention and/or Treatment of Breast/Mammary Tumorigenesis

Michael E. Grossmann, Da Qing Yang, Zhijun Guo, David A. Potter, Margot P. Cleary

Research output: Contribution to journalReview articlepeer-review

15 Scopus citations

Abstract

There is increasing interest in metformin’s effects on the development, treatment, and/or progression of breast cancer. This emerges from observational studies that diabetic women treated with metformin in comparison to other antidiabetic compounds had lower breast cancer incidence and/or mortality rates. The mechanism of action is considered to be activation of hepatic AMPK resulting in reduced gluconeogenesis. Calorie restriction, which consistently reduces mammary tumorigenesis in rodents, is also thought to act through this pathway leading to the hypothesis that metformin’s anticancer effects are mediated in a similar fashion. Here, we review the literature evaluating metformin’s anticancer effects in relation to breast/mammary tumorigenesis. We include clinical observations, as well as studies utilizing rodent models and mammary cell lines. In addition to the anticancer effect of metformin mediated through the AMPK pathway, additional mechanisms of action that directly target tissues have been identified including effects on stem cells, apoptosis, STAT3, and HER2.

Original languageEnglish (US)
Pages (from-to)312-323
Number of pages12
JournalCurrent Pharmacology Reports
Volume1
Issue number5
DOIs
StatePublished - Oct 1 2015

Bibliographical note

Funding Information:
Support for this work comes from The Hormel Foundation (MPC), NIH-NCI- R01CA157012 (MPC) and Paint the Town Pink-Grant (MPC), R01CA113570 (DAP), University of Minnesota Office of Discovery and Translation and Clinical Translational Science Institute (DAP), the Randy Shaver Cancer Foundation (DAP) and Community Fund (DAP).

Publisher Copyright:
© 2015, Springer International Publishing AG.

Keywords

  • AMPK
  • Breast cancer
  • Chemoprevention
  • Humans
  • Metformin
  • Rodents

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