Are Metformin Doses Used in Murine Cancer Models Clinically Relevant
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Collectively, these data suggest that expression levels of the uptake and extrusion transporters are not necessarily the limiting factors determining the anti-proliferative effects of metformin and that genetically determined variations in signaling pathways are variably important as are nutrient levels in the tumor microenvironment.
“Collectively, these data suggest that expression levels of the uptake and extrusion transporters are not necessarily the limiting factors determining the anti-proliferative effects of metformin and that genetically determined variations in signaling pathways are variably important as are nutrient levels in the tumor microenvironment (249, 254).”
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 [249]
Chandel et al. argue that higher concentrations of metformin are necessary in in vitro cell culture protocols because the abundance of growth factors and nutrients, such as glucose, reduces the sensitivity to the inhibitory effects of metformin.
“Chandel et al. argue that higher concentrations of metformin are necessary in in vitro cell culture protocols because the abundance of growth factors and nutrients, such as glucose, reduces the sensitivity to the inhibitory effects of metformin thus reflecting the importance of glucose and the Warburg effect for cancer cell growth as well as the importance of glycemic control in diabetes (249).”
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 [249]
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- Authors
- Chandel, N. S., Avizonis, D., Reczek, C. R., Weinberg, S. E., Menz, S., Neuhaus, R., Christian, S., Haegebarth, A., Algire, C., & Pollak, M.
- Affiliations
- Northwestern University (US)
- Bayer (Germany) (DE)
- Corresponding author
- Chandel, Navdeep S.
- Venue
- Cell Metabolism
- Publisher
- Elsevier BV
- Published
- 2016-04
- Volume
- 23
- Issue
- 4
- Pages
- 569-570
- ISSN
- 1550-4131 (ISSN-L)
- OpenAlex
- W2336052913
- Cited by
- 176
- References
- 10
- Citations by year
- 2026: 18 · 2025: 9 · 2024: 9 · 2023: 17 · 2022: 15 · 2021: 22 · 2020: 19 · 2019: 16 · 2018: 20 · 2017: 20 · 2016: 11
- FWCI
- 9.54
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Licence
- Locations
- Cell Metabolism (publishedVersion)
- PubMed (publishedVersion)
- Funders
- Cancer Research Institute
- McGill University
- Terry Fox Research Institute
- National Institutes of Health
- National Institute on Aging (P01AG049665)
- National Heart, Lung, and Blood Institute (R01HL122062, T32HL076139)
- National Cancer Institute (R01CA123067, R01 CA12306708)
- 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, AMPK, hepatic gluconeogenesis, AMPK-independent mechanism, oxidative phosphorylation inhibition, energy stress, tumor models, drug dosing, antidiabetic drugs
- MeSH terms
- Animals, Antineoplastic Agents, Disease Models, Animal, Dose-Response Relationship, Drug, Humans, Hypoglycemic Agents, Metformin, Mice, Inbred C57BL, Neoplasms, Mice
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