The antiproliferative potential and mechanism of action of metformin in MCF-7 cells

Zhibek Bekezhankyzy; Sholpan Nurzhan; Nurken Berdigaliyev; Shynggys Sergazy; Tilektes Maulenkul; Mohamad Aljofan

doi:10.2144/fsoa-2022-0080

The antiproliferative potential and mechanism of action of metformin in MCF-7 cells

Future Sci OA. 2023 Apr 21;9(5):FSO859. doi: 10.2144/fsoa-2022-0080. eCollection 2023 Jun.

Authors

Zhibek Bekezhankyzy¹, Sholpan Nurzhan¹, Nurken Berdigaliyev¹, Shynggys Sergazy², Tilektes Maulenkul³, Mohamad Aljofan^{1

2}

Affiliations

¹ Department of Biomedical Sciences, School of Medicine, Nazarbayaev University, Astana, 010000, Kazakhstan.
² National Laboratory Astana, Nazarbayev University, Astana, 010000, Kazakhstan.
³ Khoja Akhmet Yassawi International Kazakh-Turkish University, Turkistan, 161211, Turkistan, Kazakhstan.

Abstract

Aim: The current study aimed to investigate the potential antiproliferative activity of metformin, the effective concentration range, and the mechanism of action.

Materials & methods: Human breast cancer cells, MCF-7 were treated with a serial dilution of metformin (10-150 μM) for 24 and 48 h. Potential antiproliferative activity of metformin and its ability in inducing cellular apoptosis and autophagy were also investigated.

Results: Metformin inhibited MCF-7 proliferation in a concentration and time dependent manner, with 80 μM as the most effective concentration. Compared with nontreated cells, metformin induced significant levels of autophagy and apoptosis, which were confirmed by the reduction of mTOR and BCL-2 protein expression.

Conclusion: The study confirms the antiproliferative activity of metformin, which may likely occur through AMPK signaling pathway.

Keywords: antiproliferative; apoptosis; autophagy; breast cancer; metformin.

Plain language summary

The antidiabetic drug, metformin is tested in this work for its possible ability to inhibit the growth of breast cancer cells. Using different concentrations of the drug over different time points, the results showed that the drug was able to inhibit cancer growth through different mechanisms. The results also showed that the drug inhibits cancer growth by stimulating program cell death (apoptosis), as well as autophagy, where the cell breaks old and abnormal cellular substances.