Evidence map›Paper›PMID 24157871›Full record

ArticleCell death & disease2013

Contribution of serine, folate and glycine metabolism to the ATP, NADPH and purine requirements of cancer cells.

P M Tedeschi, E K Markert, M Gounder, H Lin, D Dvorzhinski, S C Dolfi, L L-Y Chan, J Qiu, R S DiPaola, K M Hirshfield and 4 more

Open access · goldAbstract read
In one paragraph

Article in Cell death & disease, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 162 papers.

0numbers the graph read from it
0cells of the map it votes in
162citing papers in PubMed
7.8field-weighted citation impact, top 2% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

162 citing papers in PubMed, 264 citations in OpenAlex.

  1. Article
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  3. Review
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  7. Article
  8. Article
  9. Article
  10. Article
  11. Article
  12. Dysregulation of Mitochondrial Function in Cancer Cells.International journal of molecular sciences · 2025
    Review
  13. Article
  14. FOLR2Cell communication and signaling : CCS · 2025
    Review
  15. Article
  16. Article
  17. Article
  18. Article
  19. Article
  20. NADPCurrent medicinal chemistry · 2025
    Review

102 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

14 authors at 2 institutions in 1 country.

P M Tedeschi1] Department of Medicine, Rutgers Cancer Institute of New Jersey, Rutgers, The State University of New Jersey, New Brunswick, NJ, USA [2] Department of Pharmacology, Rutgers Cancer Institute of New Jersey, Rutgers, The State University of New Jersey, New Brunswick, NJ, USA.
E K Markert
M Gounder
H Lin
D Dvorzhinski
S C Dolfi
L L-Y Chan
J Qiu
R S DiPaola
K M Hirshfield
L G Boros
J R Bertino
Z N Oltvai
A Vazquez
Rutgers, The State University of New Jersey · USUniversity of Pittsburgh · US

Funding

TRANSCRIPTIONAL PROFILINGP30CA072720 · NCI · UNIV OF MED/DENT NJ-R W JOHNSON MED SCH · PI Chang S Chan · 1997 to 2026
$94.5M
UMDNJ TRAINING GRANT IN BIOTECHNOLOGYT32GM008339 · NIGMS · RUTGERS THE ST UNIV OF NJ NEW BRUNSWICK · PI YARMUSH, MARTIN L · 1989 to 2019
$6.1M
NCI NIH HHS P30 CA072720NIGMS NIH HHS T32 GM008339
6 · The paper itself

Abstract

Recent observations on cancer cell metabolism indicate increased serine synthesis from glucose as a marker of poor prognosis. We have predicted that a fraction of the synthesized serine is routed to a pathway for ATP production. The pathway is composed by reactions from serine synthesis, one-carbon (folate) metabolism and the glycine cleavage system (SOG pathway). Here we show that the SOG pathway is upregulated at the level of gene expression in a subset of human tumors and that its level of expression correlates with gene signatures of cell proliferation and Myc target activation. We have also estimated the SOG pathway metabolic flux in the NCI60 tumor-derived cell lines, using previously reported exchange fluxes and a personalized model of cell metabolism. We find that the estimated rates of reactions in the SOG pathway are highly correlated with the proliferation rates of these cell lines. We also observe that the SOG pathway contributes significantly to the energy requirements of biosynthesis, to the NADPH requirement for fatty acid synthesis and to the synthesis of purines. Finally, when the PC-3 prostate cancer cell line is treated with the antifolate methotrexate, we observe a decrease in the ATP levels, AMP kinase activation and a decrease in ribonucleotides and fatty acids synthesized from [1,2-(13)C2]-D-glucose as the single tracer. Taken together our results indicate that the SOG pathway activity increases with the rate of cell proliferation and it contributes to the biosynthetic requirements of purines, ATP and NADPH of cancer cells.

Indexed as

Adenosine TriphosphateAmino Acid OxidoreductasesAnimalsCarrier ProteinsCell Line, TumorEmbryonic Stem CellsEnergy MetabolismFatty AcidsFemaleFolic AcidGene Expression Regulation, NeoplasticGlycineHumansMaleMetabolic Flux AnalysisMetabolic Networks and PathwaysAdenosine TriphosphateAmino Acid OxidoreductasesCarrier ProteinsFatty AcidsFolic AcidGlycineglycine cleavage systemMethotrexateMultienzyme ComplexesNADPpurinePurinesSerineTransferases

Identifiers

PMID24157871
PMCPMC3920946
OpenAlexW2025983003

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-SA
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.