Metformin-Mediated Glycaemic Regulation as a Potential Strategy for Breast Cancer Prevention.

[INTRODUCTION] Metformin, the common anti-hyperglycemic agent, is emerging with pharmacological significance as an effective anti-cancer modulator. Its efficacy as an anti-cancer modulator is reported in pre-clinical and clinical studies. Therefore, an attempt was made to identify the possible in vitro anti-cancer molecular mechanisms studied on breast cancer (BC) cell lines.

[METHODS] An advanced literature search was conducted in the PubMed database using search terms "Metformin, Cell culture, Breast neoplasms." Different anti-cancer molecular mechanisms induced by metformin (MET) identified in cell culture studies are presented in this paper.

[RESULTS] It was identified that MET induces molecular pathways that exert anti-cancer effects when treated on BC cells. Inhibition of oxidative phosphorylation, adenosine monophosphate-activated protein kinase mediated anticancer effects, anti-proliferation and inhibition of cell migration, alteration of tumor micro-environment, synergetic effects with conventional chemotherapies and other potential molecules, induced apoptosis and ferroptosis were mainly identified as MET-induced pathways that affect BC cells.

[CONCLUSION] Metformin induces diverse anti-cancer biochemical pathways through which it exhibits a potential to be used as an anti-cancer therapeutic in BC.