Evidence map›Paper›PMID 25241895›Full record

ArticleOncogene2015

Differential effects of AMPK agonists on cell growth and metabolism.

E E Vincent, P P Coelho, J Blagih, T Griss, B Viollet, R G Jones

Abstract read
In one paragraph

Article in Oncogene, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 88 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
88citing papers in PubMed, 1 pooled it
8.1field-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

88 citing papers in PubMed, 1 synthesis or guideline pooled it, 157 citations in OpenAlex.

  1. Pooled it
  2. Article
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  14. Article
  15. Molecular mechanisms of exercise contributing to tissue regeneration.Signal transduction and targeted therapy · 2022
    Review
  16. Article
  17. Review
  18. Article
  19. Review
  20. Article

28 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

6 authors at 3 institutions in 2 countries.

E E Vincent1] Goodman Cancer Research Centre, McGill University, Montreal, Quebec, Canada [2] Department of Physiology, McGill University, Montreal, Quebec, Canada.
P P Coelho1] Goodman Cancer Research Centre, McGill University, Montreal, Quebec, Canada [2] Department of Physiology, McGill University, Montreal, Quebec, Canada.
J Blagih1] Goodman Cancer Research Centre, McGill University, Montreal, Quebec, Canada [2] Department of Physiology, McGill University, Montreal, Quebec, Canada.
T Griss1] Goodman Cancer Research Centre, McGill University, Montreal, Quebec, Canada [2] Department of Physiology, McGill University, Montreal, Quebec, Canada.
B Viollet1] Inserm, U1016, Institut Cochin, Paris, France [2] CNRS, UMR 8104, Paris, France [3] Université Paris Descartes, Sorbonne Paris Cité, Paris, France.
R G Jones1] Goodman Cancer Research Centre, McGill University, Montreal, Quebec, Canada [2] Department of Physiology, McGill University, Montreal, Quebec, Canada.
McGill University Health Centre · CAInstitut Cochin · FRMcGill University · CA

Funding

CIHR 93799-1CIHR MOP-93799
6 · The paper itself

Abstract

As a sensor of cellular energy status, the AMP-activated protein kinase (AMPK) is believed to act in opposition to the metabolic phenotypes favored by proliferating tumor cells. Consequently, compounds known to activate AMPK have been proposed as cancer therapeutics. However, the extent to which the anti-neoplastic properties of these agonists are mediated by AMPK is unclear. Here we examined the AMPK dependence of six commonly used AMPK agonists (metformin, phenformin, 5-aminoimidazole-4-carboxamide ribonucleotide (AICAR), 2-deoxy-D-glucose (2DG), salicylate and A-769662) and their influence on cellular processes often deregulated in tumor cells. We demonstrate that the majority of these agonists display AMPK-independent effects on cell proliferation and metabolism with only the synthetic activator, A-769662, exerting AMPK-dependent effects on these processes. We find that A-769662 promotes an AMPK-dependent increase in mitochondrial spare respiratory capacity. Finally, contrary to the view of AMPK activity being tumor suppressive, we find that A-769662 confers a selective proliferative advantage to tumor cells growing under nutrient deprivation. Our results indicate that many of the antigrowth properties of these agonists cannot be attributed to AMPK activity in cells, and thus any observed effects using these agonists should be confirmed using AMPK-deficient cells. Ultimately, our data urge caution not only regarding the type of AMPK agonist proposed for cancer treatment but also the context in which they are used.

Indexed as

Adenylate KinaseAminoimidazole CarboxamideAnimalsBiphenyl CompoundsCell CycleCell Line, TumorCell ProliferationGlucoseHCT116 CellsHEK293 CellsHumansHypoglycemic AgentsLactic AcidMetforminMiceNeoplasms4-hydroxy-3-(4-(2-hydroxyphenyl)phenyl)-6-oxo-7H-thieno(2,3-b)pyridine-5-carbonitrileAdenylate KinaseAICA ribonucleotideAminoimidazole CarboxamideBiphenyl CompoundsGlucoseHypoglycemic AgentsLactic AcidMetforminPhenforminPyronesRibonucleotidesSodium SalicylateThiophenes

Identifiers

PMID25241895
PMCPMC4980123
OpenAlexW2059499603

What OpenQuestion holds

Textmetadata
LicenceTDM
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.