Modulating the therapeutic response of tumours to dietary serine and glycine starvation
Abstract
The non-essential amino acids serine and glycine are used in multiple anabolic processes that support cancer cell growth and proliferation (reviewed in ref. 1). While some cancer cells upregulate de novo serine synthesis, many others rely on exogenous serine for optimal growth. Restriction of dietary serine and glycine can reduce tumour growth in xenograft and allograft models. Here we show that this observation translates into more clinically relevant autochthonous tumours in genetically engineered mouse models of intestinal cancer (driven by Apc inactivation) or lymphoma (driven by Myc activation). The increased survival following dietary restriction of serine and glycine in these models was further improved by antagonizing the anti-oxidant response. Disruption of mitochondrial oxidative phosphorylation (using biguanides) led to a complex response that could improve or impede the anti-tumour effect of serine and glycine starvation. Notably, Kras-driven mouse models of pancreatic and intestinal cancers were less responsive to depletion of serine and glycine, reflecting an ability of activated Kras to increase the expression of enzymes that are part of the serine synthesis pathway and thus promote de novo serine synthesis.
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Restriction of dietary SG reduces tumor growth in a variety of xenografts and genetically engineered mouse models and has strong efficacy in combination with biguanides.
“Restriction of dietary SG has previously been shown to reduce tumor growth in a variety of xenografts and genetically engineered mouse models and demonstrated strong efficacy in combination with biguanides (18).”
From Eprenetapopt triggers ferroptosis, inhibits NFS1 cysteine desulfurase, and synergizes with serine and glycine dietary restriction (2022) · cites this paper as [18]
The paper reports that an SG-free diet retarded growth of HCT116 tumours and improved survival in several genetically engineered mouse models (Abstract, page unavailable). But it does not demonstrate strong efficacy with biguanides: phenformin caused marked toxicity and only a trend toward improved survival among mice that tolerated it, while metformin had no significant survival benefit and increased tumour numbers in the SG-free group (Abstract, page unavailable). (LLM, conf=0.90)
Experimental — accuracy not yet measuredPreclinical evidence supports that dietary manipulation, including SG restriction, could be a powerful adjunct to conventional therapeutic approaches.
“Preclinical evidence continues to grow, supporting the notion that dietary manipulation, including SG restriction, could be a powerful adjunct to conventional therapeutic approaches (18).”
From Eprenetapopt triggers ferroptosis, inhibits NFS1 cysteine desulfurase, and synergizes with serine and glycine dietary restriction (2022) · cites this paper as [18]
Certain tumors are dependent on uptake of environmental serine.
“Certain tumors are dependent on uptake of environmental serine (Jain et al., 2012; Maddocks et al., 2013; Maddocks et al., 2017), and limiting plasma serine availability can be beneficial for patients with these cancers.”
From Targeting Metabolism for Cancer Therapy (2017) · cites this paper as Maddocks et al., 2017
Combining serine restriction with other drugs may potentiate antitumor responses.
“Combining serine restriction with other drugs may also potentiate antitumor responses (Gravel et al., 2014; Maddocks et al., 2013; Maddocks et al., 2017).”
From Targeting Metabolism for Cancer Therapy (2017) · cites this paper as Maddocks et al., 2017
Serine deprivation by dietary restriction is sufficient to slow growth of both xenograft and autochthonous cancer models, although efficacy is influenced by the oncogenic driver mutation and tissue context.
“Additionally, serine deprivation by dietary restriction is sufficient to slow growth of both xenograft (Gravel et al., 2014; Maddocks et al., 2013) and autochthonous cancer models, although efficacy of serine deprivation appears to be influenced by both the oncogenic driver mutation and tissue context (Maddocks et al., 2017).”
From Targeting Metabolism for Cancer Therapy (2017) · cites this paper as Maddocks et al., 2017
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- Authors
- 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., Blagih, J., Vincent, D. F., Campbell, K. J., Ceteci, F., Sansom, O. J., Blyth, K., & Vousden, K. H.
- Affiliations
- Cancer Research UK Scotland Institute (GB)
- University of Glasgow (GB)
- Corresponding author
- Maddocks, Oliver D. K.
- Vousden, Karen H.
- ORCID
- Venue
- Nature
- Published
- 2017-04-20
- Volume
- 544
- Issue
- 7650
- Pages
- 372-376
- ISSN
- 0028-0836 (ISSN-L)
- 1476-4687
- OpenAlex
- W2607135274
- Cited by
- 603
- References
- 44
- Citations by year
- 2026: 41 · 2025: 60 · 2024: 72 · 2023: 75 · 2022: 86 · 2021: 82 · 2020: 82 · 2019: 59 · 2018: 26 · 2017: 20
- FWCI
- 17.55
- Type
- journal article
- Language
- en
- Update notices
- erratum (2017-08-03)
- Open access
- closed
- Locations
- Nature (publishedVersion)
- PubMed (publishedVersion)
- ENLIGHTEN (Jurnal Bimbingan dan Konseling Islam) (acceptedVersion)
- RePEc: Research Papers in Economics (submittedVersion)
- Funders
- Francis Crick Institute (10557)
- Cancer Research UK (19702, 22311, 18274, 21139)
- Beatson Institute for Cancer Research
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Cancer Research › Cancer, Hypoxia, and Metabolism
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Biochemistry › Amino Acid Enzymes and Metabolism
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Biotechnology › Cancer Research and Treatments
- Keywords
- cancer metabolism, dietary restriction, antioxidant response, de novo serine synthesis, mitochondrial oxidative phosphorylation, biguanides, MYC-driven lymphoma, genetically engineered mouse models
- MeSH terms
- Animals, Antioxidants, Biguanides, Diet, Disease Models, Animal, Female, Food Deprivation, Glycine, Humans, Intestinal Neoplasms, Lymphoma, Male, Mitochondria, Nutritional Status, Oxidative Phosphorylation, Pancreatic Neoplasms, Serine, Survival Rate, Proto-Oncogene Proteins p21(ras), Cell Line, Tumor, Mice
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
Statistics and arithmetic are recomputed, not judged.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
What counts as a claim ›How we measure confidence ›How we check this ›
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