Evidence map›Paper›PMID 29730476›Full record

ArticleNeoplasia (New York, N.Y.)2018

AICAR Antiproliferative Properties Involve the AMPK-Independent Activation of the Tumor Suppressors LATS 1 and 2.

Chloé Philippe, Benoît Pinson, Jim Dompierre, Véronique Pantesco, Benoît Viollet, Bertrand Daignan-Fornier, Michel Moenner

Open access · goldAbstract read
In one paragraph

Article in Neoplasia (New York, N.Y.), 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.

0numbers the graph read from it
0cells of the map it votes in
10citing papers in PubMed
1.3field-weighted citation impact, top 23% 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

10 citing papers in PubMed, 21 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Article
  5. Review
  6. Article
  7. Article
  8. Article
  9. Article
  10. 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

7 authors at 3 institutions in 1 country.

Chloé PhilippeUniversité de Bordeaux, IBGC UMR 5095, Bordeaux, France; Centre National de la Recherche Scientifique, IBGC UMR 5095, Bordeaux, France.
Benoît PinsonUniversité de Bordeaux, IBGC UMR 5095, Bordeaux, France; Centre National de la Recherche Scientifique, IBGC UMR 5095, Bordeaux, France.
Jim DompierreUniversité de Bordeaux, IBGC UMR 5095, Bordeaux, France; Centre National de la Recherche Scientifique, IBGC UMR 5095, Bordeaux, France.
Véronique PantescoCHU St Eloi, Montpellier, France; Inserm U1040, Montpellier, France.
Benoît ViolletINSERM U1016, Institut Cochin, Paris, France; CNRS (UMR 8104), Paris, France; Université Paris Descartes, Sorbonne Paris Cité, Paris, France.
Bertrand Daignan-FornierUniversité de Bordeaux, IBGC UMR 5095, Bordeaux, France; Centre National de la Recherche Scientifique, IBGC UMR 5095, Bordeaux, France. Electronic address: b.daignan-fornier@ibgc.cnrs.fr.
Michel MoennerUniversité de Bordeaux, IBGC UMR 5095, Bordeaux, France; Centre National de la Recherche Scientifique, IBGC UMR 5095, Bordeaux, France. Electronic address: michel.moenner@u-bordeaux.fr.
Centre National de la Recherche Scientifique · FRDélégation Paris 5 · FRInserm · FR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

AICAR (Acadesine) is a pharmacological precursor of purine nucleotide biosynthesis with anti-tumoral properties. Although recognized as an AMP mimetic activator of the protein kinase AMPK, the AICAR monophosphate derivative ZMP was also shown to mediate AMPK-independent effects. In order to unveil these AMPK-independent functions, we performed a transcriptomic analysis in AMPKα1/α2 double knockout murine embryonic cells. Kinetic analysis of the cellular response to AICAR revealed the up-regulation of the large tumor suppressor kinases (Lats) 1 and 2 transcripts, followed by the repression of numerous genes downstream of the transcriptional regulators Yap1 and Taz. This transcriptional signature, together with the observation of increased levels in phosphorylation of Lats1 and Yap1 proteins, suggested that the Hippo signaling pathway was activated by AICAR. This effect was observed in both fibroblasts and epithelial cells. Knockdown of Lats1/2 prevented the cytoplasmic delocalization of Yap1/Taz proteins in response to AICAR and conferred a higher resistance to the drug. These results indicate that activation of the most downstream steps of the Hippo cascade participates to the antiproliferative effects of AICAR.

Indexed as

Aminoimidazole CarboxamideAMP-Activated Protein KinasesAnimalsAntineoplastic AgentsCell ProliferationCells, CulturedEnzyme ActivationEpithelial CellsFibroblastsHumansMiceMice, KnockoutPhosphoproteinsProtein Serine-Threonine KinasesRibonucleosidesSignal TransductionacadesineAminoimidazole CarboxamideAMP-Activated Protein KinasesAntineoplastic AgentsLATS1 protein, humanLATS2 protein, humanPhosphoproteinsProtein Serine-Threonine KinasesRibonucleosidesTranscription FactorsTumor Suppressor Proteins

Identifiers

PMID29730476
PMCPMC5994775
OpenAlexW2800427169

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.