Co-treatment of breast cancer cells with pharmacologic doses of 2-deoxy-D-glucose and metformin: Starving tumors
Open accessAbstract
A characteristic of tumor cells is the increased aerobic glycolysis for energy production. Thus, inhibition of glycolysis represents a selective therapeutic option. It has been shown that glycolysis inhibitor 2-deoxy-D-glucose (2DG) induces apoptotic cell death in different tumor entities. In addition, the antitumor activity of the anti-diabetic drug metformin has been demonstrated. In the present study, we aimed to ascertain whether the combination of pharmacologic doses of 2DG with metformin increases the antitumor efficacy. Cell viability of MDA-MB-231 and HCC1806 triple-negative breast cancer (TNBC) cells treated without or with 2DG or with metformin alone or with the combination of both agents was measured using Alamar Blue assay. Induction of apoptosis was quantified by measurement of the loss of mitochondrial membrane potential and cleavage of PARP. Treatment of breast cancer cells with glycolysis inhibitor 2DG or with the anti-diabetic drug metformin resulted in a significant decrease in cell viability and an increase in apoptosis. Treatment with 2DG in combination with metformin resulted in significantly reduced viability compared with the single agent treatments. The observed reduction in viability was due to induction of apoptosis. In addition, in regards to apoptosis induction a stronger effect in the case of co-treatment compared with single agent treatments was observed. The glycolytic phenotype of human breast cancer cells can be targeted for therapeutic intervention. Co-treatment with doses of the glycolysis inhibitor 2DG and anti-diabetic drug metformin is tolerable in humans and may be a suitable therapy for human breast cancers.
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2-DG is a promising inhibitor of glycolysis that decreases energy of cancer cells, making chemotherapy and other treatments more effective, and is most likely useful for treatment of breast cancer including TNBC.
“2-DG is a promising inhibitor of glycolysis, which decreases the energy of the cancer cells thus making chemotherapy and other treatments more effective. It underwent clinical trials and most likely is useful for the treatment of breast cancer including TNBC (Wokoun et al., 2017; Lucantoni et al., 2018; O’Neill et al., 2019).”
From An Arthropod Hormone, Ecdysterone, Inhibits the Growth of Breast Cancer Cells via Different Mechanisms (2020) · cites this paper as Wokoun et al., 2017
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References 39 · Cited by 45
- Authors
- Wokoun, U., Hellriegel, M., Emons, G., & Gründker, C.
- Affiliations
- University of Göttingen (DE)
- Venue
- Oncology Reports
- Publisher
- Spandidos Publications
- Published
- 2017-03
- Volume
- 37
- Issue
- 4
- Pages
- 2418-2424
- ISSN
- 1021-335X (ISSN-L)
- 1791-2431
- OpenAlex
- W2592652268
- Cited by
- 45
- References
- 39
- Citations by year
- 2026: 2 · 2025: 2 · 2024: 8 · 2023: 1 · 2022: 8 · 2021: 7 · 2020: 9 · 2019: 7 · 2017: 1
- FWCI
- 1.90
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- Oncology Reports (publishedVersion)
- PubMed (publishedVersion)
- Funders
- Deutsche Krebshilfe (111027)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Metabolism, Diabetes, and Cancer
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Cancer Research › Cancer, Hypoxia, and Metabolism
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › PI3K/AKT/mTOR signaling in cancer
- Keywords
- 2-deoxyglucose, metformin, triple-negative breast cancer, aerobic glycolysis, glycolysis inhibition, combination therapy, apoptosis, mitochondrial membrane potential, PARP cleavage, MDA-MB-231 cells, HCC1806, antitumor efficacy
- MeSH terms
- Antineoplastic Combined Chemotherapy Protocols, Cell Survival, Deoxyglucose, Dose-Response Relationship, Drug, Drug Synergism, Female, Glycolysis, Humans, Metformin, Poly(ADP-ribose) Polymerases, Gene Expression Regulation, Neoplastic, Apoptosis, Cell Line, Tumor, Cell Proliferation, Membrane Potential, Mitochondrial, Triple Negative Breast Neoplasms
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