Metformin as an Anticancer Agent
Open accessAbstract
Metformin has been a frontline therapy for type 2 diabetes (T2D) for many years. Its effectiveness in T2D treatment is mostly attributed to its suppression of hepatic gluconeogenesis; however, the mechanistic aspects of metformin action remain elusive. In addition to its glucose-lowering effect, metformin possesses other pleiotropic health-promoting effects that include reduced cancer risk and tumorigenesis. Metformin inhibits the electron transport chain (ETC) and ATP synthesis; however, recent data reveal that metformin regulates AMP-activated protein kinase (AMPK) and the mechanistic target of rapamycin complex 1 (mTORC1) by multiple, mutually nonexclusive mechanisms that do not necessarily depend on the inhibition of ETC and the cellular ATP level. In this review, we discuss recent advances in elucidating the molecular mechanisms that are relevant for metformin use in cancer treatment.
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Extensive support for a protective effect of metformin against cancer has been provided by numerous, but not all studies.
“Extensive support for a protective effect of metformin against cancer has been provided by numerous, but not all studies (237, 238).”
From A Critical Review of the Evidence That Metformin Is a Putative Anti-Aging Drug That Enhances Healthspan and Extends Lifespan (2021) · cites this paper as [238]
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- Authors
- Vancura, A., Bu, P., Bhagwat, M., Zeng, J., & Vancurova, I.
- Affiliations
- St. John's University (US)
- Venue
- Trends in Pharmacological Sciences
- Publisher
- Elsevier BV
- Published
- 2018-10
- Volume
- 39
- Issue
- 10
- Pages
- 867-878
- ISSN
- 0165-6147 (ISSN-L)
- PMC
- PMC6153060
- OpenAlex
- W2888538492
- Cited by
- 274
- References
- 107
- Citations by year
- 2026: 14 · 2025: 29 · 2024: 34 · 2023: 40 · 2022: 47 · 2021: 39 · 2020: 41 · 2019: 30
- FWCI
- 2.69
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Licence
- Locations
- Trends in Pharmacological Sciences (acceptedVersion)
- PubMed (publishedVersion)
- PubMed Central (acceptedVersion)
- Funders
- NIH (GM120710)
- 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
- metformin, anticancer effects, type 2 diabetes, AMPK, mTORC1, electron transport inhibition, ATP production, hepatic gluconeogenesis, cancer risk reduction, carcinogenesis, pleiotropy
- MeSH terms
- Mechanistic Target of Rapamycin Complex 1, Animals, Antineoplastic Agents, Diabetes Mellitus, Type 2, Humans, Hypoglycemic Agents, Metformin, Neoplasms, Electron Transport Complex I, AMP-Activated Protein Kinases
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