Cited by 176Metabolism, Diabetes, and CancerCancer, Hypoxia, and MetabolismPI3K/AKT/mTOR signaling in cancer

Are Metformin Doses Used in Murine Cancer Models Clinically Relevant

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Chandel, Navdeep S., Avizonis, Dania, Reczek, Colleen R., Weinberg, Samuel E., Menz, Stephan, Neuhaus, Roland, Christian, Sven, Haegebarth, Andrea +2 more·2016·Cell Metabolism

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Crossref · 10.1016/j.cmet.2016.03.010

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10 of 10 references verified0 citation errors · 0 not checkable

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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).”
  • 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).”

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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
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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