Metformin induces unique biological and molecular responses in triple negative breast cancer cells
Open accessAbstract
Triple negative (TN) breast cancer is more frequent in women who are obese or have type II diabetes, as well as young women of color. These cancers do not express receptors for the steroid hormones estrogen or progesterone, or the type II receptor tyrosine kinase (RTK) Her-2 but do have upregulation of basal cytokeratins and the epidermal growth factor receptor (EGFR). These data suggest that aberrations of glucose and fatty acid metabolism, signaling through EGFR and genetic factors may promote the development of TN cancers. The anti-type II diabetes drug metformin has been associated with a decreased incidence of breast cancer, although the specific molecular subtypes that may be reduced by metformin have not been reported. Our data indicates that metformin has unique anti-TN breast cancer effects both in vitro and in vivo. It inhibits cell proliferation (with partial S phase arrest), colony formation and induces apoptosis via activation of the intrinsic and extrinsic signaling pathways only in TN breast cancer cell lines. At the molecular level, metformin increases P-AMPK, reduces P-EGFR, EGFR, P-MAPK, P-Src, cyclin D1 and cyclin E (but not cyclin A or B, p27 or p21), and induces PARP cleavage in a dose- and time-dependent manner. These data are in stark contrast to our previously published biological and molecular effects of metformin on luminal A and B, or Her-2 type breast cancer cells. Nude mice bearing tumor xenografts of the TN line MDA-MB-231, treated with metformin, show significant reductions in tumor growth (p = 0.0066) and cell proliferation (p = 0.0021) as compared to untreated controls. Metformin pre-treatment, before injection of MDA-MB-231 cells, results in a significant decrease in tumor outgrowth and incidence. Given the unique anti-cancer activity of metformin against TN disease, both in vitro and in vivo, it should be explored as a therapeutic agent against this aggressive form of breast cancer.
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In laboratory studies, metformin inhibits cell proliferation, reduces colony formation, and causes partial cell cycle arrest in cancer cell lines.
“In laboratory studies, metformin has been shown to inhibit cell proliferation, reduce colony formation, and cause partial cell cycle arrest in cancer cell lines (81–83).”
From Diabetes and Cancer (2010) · cites this paper as [83]
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- Authors
- Liu, B., Fan, Z., Edgerton, S. M., Deng, X.-S., Alimova, I. N., Lind, S. E., & Thor, A. D.
- Affiliations
- University of Colorado Anschutz (US)
- University of Colorado Denver (US)
- Venue
- Cell Cycle
- Publisher
- Informa UK Limited
- Published
- 2009-07
- Volume
- 8
- Issue
- 13
- Pages
- 2031-2040
- ISSN
- 1538-4101 (ISSN-L)
- 1551-4005
- OpenAlex
- W2108183713
- Cited by
- 392
- References
- 53
- Citations by year
- 2026: 2 · 2025: 7 · 2024: 5 · 2023: 10 · 2022: 13 · 2021: 12 · 2020: 25 · 2019: 21 · 2018: 18 · 2017: 31 · 2016: 29 · 2015: 35 · 2014: 37 · 2013: 33 · 2012: 35
- FWCI
- 15.28
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- Cell Cycle (publishedVersion)
- PubMed (publishedVersion)
- Funders
- Avon Foundation for Women
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Metabolism, Diabetes, and Cancer
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › PI3K/AKT/mTOR signaling in cancer
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Cancer Research › Cancer, Hypoxia, and Metabolism
- Keywords
- metformin, triple-negative breast cancer, EGFR signaling, AMPK, mitogen-activated protein kinase, Src kinase, cyclin D1, cyclin E, apoptosis, cell proliferation, tumor xenografts, MDA-MB-231 cells, PARP cleavage, anticancer drug repurposing
- MeSH terms
- Animals, Antineoplastic Agents, Breast Neoplasms, Cell Cycle, Female, Humans, Metformin, Mice, Nude, Poly(ADP-ribose) Polymerases, Tumor Cells, Cultured, Signal Transduction, Apoptosis, Caspases, Xenograft Model Antitumor Assays, Cell Proliferation, Mice, AMP-Activated Protein Kinases
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