Evidence map›Paper›PMID 28916747›Full record

ArticleScientific reports2017

Hormetic potential of methylglyoxal, a side-product of glycolysis, in switching tumours from growth to death.

Marie-Julie Nokin, Florence Durieux, Justine Bellier, Olivier Peulen, Koji Uchida, David A Spiegel, James R Cochrane, Craig A Hutton, Vincent Castronovo, Akeila Bellahcène

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 59 papers.

0numbers the graph read from it
0cells of the map it votes in
59citing papers in PubMed
4.7field-weighted citation impact, top 5% 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

59 citing papers in PubMed, 80 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Article
  5. Article
  6. Article
  7. Article
  8. Review
  9. Article
  10. Article
  11. Article
  12. Review
  13. Article
  14. Review
  15. Review
  16. Article
  17. Article
  18. Recruited atypical Ly6GScience immunology · 2024
    Article
  19. Review
  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

10 authors at 4 institutions in 4 countries.

Marie-Julie NokinMetastasis Research Laboratory, GIGA-CANCER, University of Liège, Liège, Belgium.
Florence DurieuxMetastasis Research Laboratory, GIGA-CANCER, University of Liège, Liège, Belgium.
Justine BellierMetastasis Research Laboratory, GIGA-CANCER, University of Liège, Liège, Belgium.
Olivier PeulenMetastasis Research Laboratory, GIGA-CANCER, University of Liège, Liège, Belgium.
Koji UchidaLaboratory of Food Chemistry, Department of Applied Biological Chemistry, Graduate School of Agricultural and Life Sciences, University of Tokyo, Tokyo, Japan.
David A SpiegelDepartment of Chemistry, Yale University, 225 Prospect Street, New Haven, Connecticut, USA.
James R CochraneSchool of Chemistry and Bio21 Molecular Science and Biotechnology Institute, University of Melbourne, Melbourne, Australia.
Craig A HuttonSchool of Chemistry and Bio21 Molecular Science and Biotechnology Institute, University of Melbourne, Melbourne, Australia.
Vincent CastronovoMetastasis Research Laboratory, GIGA-CANCER, University of Liège, Liège, Belgium.
Akeila BellahcèneMetastasis Research Laboratory, GIGA-CANCER, University of Liège, Liège, Belgium. a.bellahcene@ulg.ac.be.
University of Liège · BEUniversity of Melbourne · AUThe University of Tokyo · JPYale University · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Metabolic reprogramming toward aerobic glycolysis unavoidably favours methylglyoxal (MG) and advanced glycation end products (AGEs) formation in cancer cells. MG was initially considered a highly cytotoxic molecule with potential anti-cancer value. However, we have recently demonstrated that MG enhanced tumour growth and metastasis. In an attempt to understand this dual role, we explored MG-mediated dicarbonyl stress status in four breast and glioblastoma cancer cell lines in relation with their glycolytic phenotype and MG detoxifying capacity. In glycolytic cancer cells cultured in high glucose, we observed a significant increase of the conversion of MG to D-lactate through the glyoxalase system. Moreover, upon exogenous MG challenge, glycolytic cells showed elevated amounts of intracellular MG and induced de novo GLO1 detoxifying enzyme and Nrf2 expression. Thus, supporting the adaptive nature of glycolytic cancer cells to MG dicarbonyl stress when compared to non-glycolytic ones. Finally and consistent with the pro-tumoural role of MG, we showed that low doses of MG induced AGEs formation and tumour growth in vivo, both of which can be reversed using a MG scavenger. Our study represents the first demonstration of a hormetic effect of MG defined by a low-dose stimulation and a high-dose inhibition of tumour growth.

Indexed as

Cell ProliferationGlycolysisHormesisCell DeathCell Line, TumorGlycation End Products, AdvancedHumansLactoylglutathione LyaseNeoplasmsNF-E2-Related Factor 2PyruvaldehydeGLO1 protein, humanGlycation End Products, AdvancedLactoylglutathione LyaseNFE2L2 protein, humanNF-E2-Related Factor 2Pyruvaldehyde

Identifiers

PMID28916747
PMCPMC5600983
OpenAlexW2756143739

What OpenQuestion holds

Textmetadata
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.