Do MCF7 cells cope with metformin treatment under energetic stress in low glucose conditions?

Dogan Turacli I., UMUDUM H., Pampal A., Candar T., Kavasoglu L., Sari Y.

Molecular Biology Reports, vol.45, no.3, pp.195-201, 2018 (SCI-Expanded) identifier identifier identifier

  • Publication Type: Article / Article
  • Volume: 45 Issue: 3
  • Publication Date: 2018
  • Doi Number: 10.1007/s11033-018-4152-5
  • Journal Name: Molecular Biology Reports
  • Journal Indexes: Science Citation Index Expanded (SCI-EXPANDED), Scopus
  • Page Numbers: pp.195-201
  • Keywords: Breast cancer, Estrogen receptor, Galectin-3, Low glucose, Metformin, Progesterone receptor, CANCER-CELLS, BREAST-CANCER, ANTIDIABETIC DRUG, METABOLISM, THERAPY, AMPK, TUMORIGENESIS, INHIBITION, ACTIVATION, KINASE
  • Lokman Hekim University Affiliated: No


© 2018, Springer Science+Business Media B.V., part of Springer Nature.There is a growing body of evidence about metformin being effective in cancer therapy. Despite controversies about the ways of its effectiveness, several ongoing clinical trials are evaluating the drug when used as an adjuvant or a neo-adjuvant agent. We aimed to investigate metformin’s effects on proliferation, metastasis, and hormone receptor expressions in breast cancer cell line MCF-7 incubated in two different glucose conditions. MCF-7 cells were incubated in high or low glucose media and treated with various doses of metformin. The cell viability was studied using MTT test. The Ki-67, estrogen and progesterone receptor expression were evaluated by ICC and galectin-3 expression was evaluated by ELISA or spectrophotometrically. The cell viability following consecutive metformin doses in either glucose condition for 24 and 48 h represented a significant decrease when compared to control. The proliferation detected in low glucose medium following metformin at doses < 20 mM was found significantly decreased when compared to high glucose medium at 48 h. In terms of galectin-3 levels, the increase in high glucose medium treated with metformin and the decrease in low glucose medium were found statistically significant when compared to control. Progesterone receptor staining demonstrated a significant increase in low glucose medium. Our findings represent better outcomes for cancer lines incubated in low glucose medium treated with metformin in terms of viability, receptor expression and metastatic activity, and highlight the potential benefit of metformin especially in restraining the cancer cell’s ability to cope energetic stress in low glucose conditions.