The DOI matches its Crossref record; 10 of the 10 references it cites were found in a registry or an index.
Are Metformin Doses Used in Murine Cancer Models Clinically Relevant
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In the citing paper
“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]
In the citing paper
“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]
Citations
Cites
Metformin: from mechanisms of action to therapies
Foretz, M., Guigas, B., Bertrand, L., Pollak, M., & Viollet, B. (2014) · Cell Metabolism · doi:10.1016/j.cmet.2014.09.018 · Cited by 1,501
Clinical pharmacokinetics of metformin
Graham, G. G., Punt, J., Arora, M., Day, R. O., Doogue, M. P., Duong, J. K., Furlong, T. J., Greenfield, J. R., Greenup, L. C., Kirkpatrick, C. M., et al. (2011) · Clinical Pharmacokinetics · doi:10.2165/11534750-000000000-00000 · Cited by 1,318
Metformin inhibits mitochondrial complex I of cancer cells to reduce tumorigenesis
Wheaton, W. W., Weinberg, S. E., Hamanaka, R. B., Soberanes, S., Sullivan, L. B., Anso, E., Glasauer, A., Dufour, E., Mutlu, G. M., Budigner, G. S., et al. (2014) · eLife · doi:10.7554/elife.02242 · Cited by 1,105
Buzzai, M., Jones, R. G., Amaravadi, R. K., Lum, J. J., DeBerardinis, R. J., Zhao, F., Viollet, B., & Thompson, C. B. (2007) · Cancer Research · doi:10.1158/0008-5472.can-06-4447 · Cited by 949
Metabolic determinants of cancer cell sensitivity to glucose limitation and biguanides
Birsoy, K., Possemato, R., Lorbeer, F. K., Bayraktar, E. C., Thiru, P., Yucel, B., Wang, T., Chen, W. W., Clish, C. B., & Sabatini, D. M. (2014) · Nature · doi:10.1038/nature13110 · Cited by 710
Metformin Action: Concentrations Matter
He, L., & Wondisford, F. E. (2015) · Cell Metabolism · doi:10.1016/j.cmet.2015.01.003 · Cited by 448
Kordes, S., Pollak, M. N., Zwinderman, A. H., Mathôt, R. A., Weterman, M. J., Beeker, A., Punt, C. J., Richel, D. J., & Wilmink, J. W. (2015) · The Lancet Oncology · doi:10.1016/s1470-2045(15)00027-3 · Cited by 361
Lévy, J., Cacheux, W., Bara, M. A., L’Hermitte, A., Lepage, P., Fraudeau, M., Trentesaux, C., Lemarchand, J., Durand, A., Crain‐Denoyelle, A., et al. (2015) · Nature Cell Biology · doi:10.1038/ncb3206 · Cited by 200
Algire, C., Amrein, L., Bazile, M., David, S., Zakikhani, M., & Pollak, M. (2010) · Oncogene · doi:10.1038/onc.2010.483 · Cited by 186
Serine deprivation enhances antineoplastic activity of biguanides
Gravel, S.-P., Hulea, L., Toban, N., Birman, E., Blouin, M.-J., Zakikhani, M., Zhao, Y., Topisirovic, I., St-Pierre, J., & Pollak, M. (2014) · Cancer Research · doi:10.1158/0008-5472.can-14-2643-t · Cited by 138
Self-citation
Cited by
Sorted by citations
Cellular and Molecular Mechanisms of Metformin Action
LaMoia, T. E., & Shulman, G. I. (2021) · Endocrine Reviews · doi:10.1210/endrev/bnaa023 · Cited by 791
“…metformin in rodents with ad libitum access to metformin-treated drinking water results in inconsistent plasma metformin concentrations, possibly due to variability in drinking and/or absorption from the gut, with studies reporting plasma concentrations ranging from 5 µ M to 180 µ M (48, 52, 53).”
BackgroundMitochondrial Metabolism as a Target for Cancer Therapy
Vasan, K., Werner, M., & Chandel, N. S. (2020) · Cell Metabolism · doi:10.1016/j.cmet.2020.06.019 · Cited by 762
Metformin: update on mechanisms of action and repurposing potential
Foretz, M., Guigas, B., & Viollet, B. (2023) · Nature Reviews Endocrinology · doi:10.1038/s41574-023-00833-4 · Cited by 791
Modulating the therapeutic response of tumours to dietary serine and glycine starvation
Maddocks, O. D. K., Athineos, D., Cheung, E. C., Lee, P., Zhang, T., van den Broek, N. J. F., Mackay, G. M., Labuschagne, C. F., Gay, D., Kruiswijk, F., et al. (2017) · Nature · doi:10.1038/nature22056 · Cited by 603
Hallmarks of cancer stem cell metabolism
Sancho, P., Barneda, D., & Heeschen, C. (2016) · British Journal of Cancer · doi:10.1038/bjc.2016.152 · Cited by 596
“…Journal of Cancer (2016) 114, 1305–1312 | doi: 10.1038/bjc.2016.152 www.bjcancer.com | DOI:10.1038/bjc.2016.152 1305 Second, cancer heterogeneity also exists within each of these subclones, despite their identical genetic background, via the acquisition of stemness features in a subset of cells.”
BackgroundInfluential
Metadata
- 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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