Evidence map›Paper›PMID 23460817›Full record

ArticlePloS one2013

Warburg and Crabtree effects in premalignant Barrett's esophagus cell lines with active mitochondria.

Martin T Suchorolski, Thomas G Paulson, Carissa A Sanchez, David Hockenbery, Brian J Reid

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.

0numbers the graph read from it
0cells of the map it votes in
25citing papers in PubMed
1.3field-weighted citation impact, top 20% 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

25 citing papers in PubMed, 39 citations in OpenAlex.

  1. Trial
  2. Review
  3. Article
  4. O-GlcNAcylation: Crosstalk between Hemostasis, Inflammation, and Cancer.International journal of molecular sciences · 2024
    Review
  5. Review
  6. The role of Glut-1 and HEuropean archives of oto-rhino-laryngology : official journal of the European Federation of Oto-Rhino-Laryngological Societies (EUFOS) : affiliated with the German Society for Oto-Rhino-Laryngology - Head and Neck Surgery · 2022
    Article
  7. Article
  8. Article
  9. Article
  10. Review
  11. Review
  12. Review
  13. Article
  14. Germline BAP1 mutations induce a Warburg effect.Cell death and differentiation · 2017
    Article
  15. MitochondrialThe Journal of biological chemistry · 2017
    Article
  16. Article
  17. Article
  18. Article
  19. Monomethylarsonous acid, but not inorganic arsenic, is a mitochondria-specific toxicant in vascular smooth muscle cells.Toxicology in vitro : an international journal published in association with BIBRA · 2016
    Article
  20. Article
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

5 authors at 2 institutions in 1 country.

Martin T SuchorolskiMolecular and Cellular Biology Department, University of Washington, Seattle, Washington, United States of America. msuchoro@uw.edu
Thomas G Paulson
Carissa A Sanchez
David Hockenbery
Brian J Reid
Fred Hutch Cancer Center · USUniversity of Washington · US

Funding

CEGSTech: Integrated Biologically-Active MicrosystemsP50HG002360 · NHGRI · UNIVERSITY OF WASHINGTON · PI MELDRUM, DEIRDRE R. · 2001 to 2012
$37.8M
PHYLOGENIES of Barrett's Esophagus LineagesP01CA091955 · NCI · FRED HUTCHINSON CANCER RESEARCH CENTER · PI GRADY, WILLIAM MALLORY · 2002 to 2019
$35.9M
NCI NIH HHS P01 CA091955NCI NIH HHS P01 CA91955NHGRI NIH HHS 1 P50HG02360NHGRI NIH HHS P50 HG002360
6 · The paper itself

Abstract

backgroundIncreased glycolysis is a hallmark of cancer metabolism, yet relatively little is known about this phenotype at premalignant stages of progression. Periodic ischemia occurs in the premalignant condition Barrett's esophagus (BE) due to tissue damage from chronic acid-bile reflux and may select for early adaptations to hypoxia, including upregulation of glycolysis. METHODOLOGY/PRINCIPAL

findingsWe compared rates of glycolysis and oxidative phosphorylation in four cell lines derived from patients with BE (CP-A, CP-B, CP-C and CP-D) in response to metabolic inhibitors and changes in glucose concentration. We report that cell lines derived from patients with more advanced genetically unstable BE have up to two-fold higher glycolysis compared to a cell line derived from a patient with early genetically stable BE; however, all cell lines preserve active mitochondria. In response to the glycolytic inhibitor 2-deoxyglucose, the most glycolytic cell lines (CP-C and CP-D) had the greatest suppression of extra-cellular acidification, but were able to compensate with upregulation of oxidative phosphorylation. In addition, these cell lines showed the lowest compensatory increases in glycolysis in response to mitochondrial uncoupling by 2,4-dinitrophenol. Finally, these cell lines also upregulated their oxidative phosphorylation in response to glucose via the Crabtree effect, and demonstrate a greater range of modulation of oxygen consumption. CONCLUSIONS/SIGNIFICANCE: Our findings suggest that cells from premalignant Barrett's esophagus tissue may adapt to an ever-changing selective microenvironment through changes in energy metabolic pathways typically associated with cancer cells.

Indexed as

Models, Biological2,4-DinitrophenolAcidsBarrett EsophagusCell Line, TumorDeoxyglucoseDisease ProgressionEnergy MetabolismExtracellular SpaceGenomic InstabilityGlycolysisHumansMitochondriaNeoplasm StagingOxidative PhosphorylationOxygen Consumption2,4-DinitrophenolAcidsDeoxyglucoseUncoupling Agents

Identifiers

PMID23460817
PMCPMC3584058
OpenAlexW2083667106

What OpenQuestion holds

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LicenceCC BY
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.