Abstract
A whole new area of investigation has emerged recently with regards to the anti-diabetic drug metformin and breast cancer. Metformins anti-breast cancer actions, observed in population studies, in rodents and in cultured tumour cells, are especially encouraging because they attack not only the most common bulk of the tumour cells but also the more rare tumour-initiating stem cells. Here, we illustrate the multifaceted and redundant mechanisms through which metformin-reprogrammed energy metabolism at both the organismal and cellular levels constitutes a novel and valuable strategy to prevent and treat breast cancer disease.
Keywords: Insulin, Diabetes, Metformin, Breast cancer, AMPK, Stem cells, Carcinogenesis, Hyperinsulinaemia, Biguanide derivative, Inflammation, Oestrogen, Apoptosis, IGF, Tumouricidal effect, Neoplasias, Adenocarcinomas, Thiazolidinediones, Sulfonylureas, Glibenclamide, Chemotherapy, Gluconeogenesis, Insulinaemia, Aerobic glycolysis, Oxidative phosphorylation, Mitosis, Glucose tolerance, Aromatase expression, Tyrosine kinase inhibitors, Antibodies, Supplementation, Lapatinib, Trastuzumab, Anti-HER2 therapy, PARP inhibitors, EGFR, Anti-cancer drugs, Cytotoxics, Anthracycline doxorubicin
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