Evidence map›Paper›PMID 28724379›Full record

ArticleJournal of translational medicine2017

Regulation of glucose uptake in lymphoma cell lines by c-MYC- and PI3K-dependent signaling pathways and impact of glycolytic pathways on cell viability.

Martina Broecker-Preuss, Nina Becher-Boveleth, Andreas Bockisch, Ulrich Dührsen, Stefan Müller

Open access · goldAbstract read
In one paragraph

Article in Journal of translational medicine, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers.

0numbers the graph read from it
0cells of the map it votes in
34citing papers in PubMed
2.4field-weighted citation impact, top 11% 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

34 citing papers in PubMed, 52 citations in OpenAlex.

  1. Review
  2. Review
  3. The Warburg Effect and Aerobic Glycolysis in Tumors.Cancer treatment and research · 2026
    Review
  4. Review
  5. Article
  6. Review
  7. Review
  8. Review
  9. Article
  10. Review
  11. Metabolic Reprogramming and Potential Therapeutic Targets in Lymphoma.International journal of molecular sciences · 2023
    Review
  12. Review
  13. Article
  14. Metabolism in Hematopoiesis and Its Malignancy.Advances in experimental medicine and biology · 2023
    Article
  15. Article
  16. Article
  17. Review
  18. Article
  19. Review
  20. Review
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 1 institution in 1 country.

Martina Broecker-PreussDepartment of Nuclear Medicine, University Hospital Essen, Hufelandstr. 55, 45122, Essen, Germany. martina.broecker@uni-due.de.ORCID 0000-0003-4537-0964
Nina Becher-BovelethDepartment of Nuclear Medicine, University Hospital Essen, Hufelandstr. 55, 45122, Essen, Germany.
Andreas BockischDepartment of Nuclear Medicine, University Hospital Essen, Hufelandstr. 55, 45122, Essen, Germany.
Ulrich DührsenDepartment of Hematology, University Hospital Essen, Hufelandstr. 55, 45122, Essen, Germany.
Stefan MüllerDepartment of Nuclear Medicine, University Hospital Essen, Hufelandstr. 55, 45122, Essen, Germany.
Essen University Hospital · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundChanges in glucose and energy metabolism contribute to the altered phenotype of cancer cells and are the basis for positron emission tomography with

methodsAn FDG uptake assay was established and uptake of FDG by lymphoma cells was determined after incubation with inhibitors of the c-MYC and the PI3K signalling pathways that are known to be activated in lymphoma cells and able to regulate glucose metabolism. Inhibitors of MAPK signalling pathways whose role in altered metabolism is still unclear were also investigated. Expression of mRNAs of the glucose transporter 1 (GLUT1), hexokinase 2 (HK2), glucose-6-phosphatase (G6Pase) and lactate dehydrogenase A (LDHA) and of the glucose metabolism-regulating micro RNAs (miRNA) miR21, -23a, -133a, -133b, -138-1 and -143 was determined by RT-PCR. Cell viability was analysed by MTT assay.

resultsTreatment with the c-MYC inhibitor 10058-F4 and inhibitors of the PI3K/mTOR pathway diminished uptake of FDG in all three cell lines, while inhibition of MAPK pathways had no effect on glucose uptake. Expression of glycolysis-related genes and miRNAs were diminished, although to a variable degree in the three cell lines. The c-MYC inhibitor, the PI3K inhibitor LY294002, the mTOR inhibitor Rapamycin and 2-DG all diminished the number of viable cells. Interestingly, in combination with 2-DG, the c-MYC inhibitor, LY294002 and the p38 MAPK inhibitor SB203580 had synergistic effects on cell viability in all three cell lines.

conclusionsc-MYC- and PI3K/mTOR-inhibitors decreased viability of the lymphoma cells and led to decreased glucose uptake, expression of glycolysis-associated genes, and glucose metabolism-regulating miRNAs. Inhibition of HK by 2-DG reduced cell numbers as a single agent and synergistically with inhibitors of other intracellular pathways. Thus, targeted inhibition of the pathways investigated here could be a strategy to suppress the glycolytic phenotype of lymphoma cells and reduce proliferation.

Indexed as

GlycolysisCell Line, TumorCell SurvivalChromonesFluorodeoxyglucose F18GlucoseHumansInhibitory Concentration 50LymphomaMorpholinesPhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-mycSirolimusTime Factors2-(4-morpholinyl)-8-phenyl-4H-1-benzopyran-4-oneChromonesFluorodeoxyglucose F18GlucoseMorpholinesPhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-mycSirolimus18F-fluoro-2-deoxy-D-glucose2-deoxy-D-glucoseGlucose metabolismLymphomaWarburg effect

Identifiers

PMID28724379
PMCPMC5517804
OpenAlexW2737280983

What OpenQuestion holds

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LicenceCC BY
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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.