Evidence map›Paper›PMID 32234473›Full record

ArticleCell reports2020

Nutlin-Induced Apoptosis Is Specified by a Translation Program Regulated by PCBP2 and DHX30.

Dario Rizzotto, Sara Zaccara, Annalisa Rossi, Matthew D Galbraith, Zdenek Andrysik, Ahwan Pandey, Kelly D Sullivan, Alessandro Quattrone, Joaquín M Espinosa, Erik Dassi and 1 more

Open access · goldAbstract read
In one paragraph

Article in Cell reports, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed
1.6field-weighted citation impact, top 17% 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

22 citing papers in PubMed, 31 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. PCBP2 in gastrointestinal cancers: fundamental mechanism and clinical potential.Journal of molecular medicine (Berlin, Germany) · 2025
    Review
  5. Article
  6. Article
  7. Article
  8. Article
  9. Article
  10. Article
  11. Structural Basis of Mutation-Dependent p53 Tetramerization Deficiency.International journal of molecular sciences · 2022
    Article
  12. Review
  13. Article
  14. Review
  15. iScience · 2021
    Article
  16. Review
  17. Article
  18. 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

11 authors at 3 institutions in 2 countries.

Dario RizzottoDepartment of Cellular, Computational and Integrative Biology (CIBIO), University of Trento, via Sommarive 9, 38123 Trento, Italy.
Sara ZaccaraDepartment of Cellular, Computational and Integrative Biology (CIBIO), University of Trento, via Sommarive 9, 38123 Trento, Italy.
Annalisa RossiDepartment of Cellular, Computational and Integrative Biology (CIBIO), University of Trento, via Sommarive 9, 38123 Trento, Italy.
Matthew D GalbraithLinda Crnic Institute for Down Syndrome, University of Colorado Anschutz Medical Campus, Aurora, CO 80045, USA; Department of Pharmacology, University of Colorado Anschutz Medical Campus, Aurora, CO 80045, USA; Department of Molecular, Cellular and Developmental Biology, University of Colorado, Boulder, Boulder, CO 80203, USA.
Zdenek AndrysikLinda Crnic Institute for Down Syndrome, University of Colorado Anschutz Medical Campus, Aurora, CO 80045, USA; Department of Pharmacology, University of Colorado Anschutz Medical Campus, Aurora, CO 80045, USA; Department of Molecular, Cellular and Developmental Biology, University of Colorado, Boulder, Boulder, CO 80203, USA.
Ahwan PandeyLinda Crnic Institute for Down Syndrome, University of Colorado Anschutz Medical Campus, Aurora, CO 80045, USA; Department of Pharmacology, University of Colorado Anschutz Medical Campus, Aurora, CO 80045, USA; Department of Molecular, Cellular and Developmental Biology, University of Colorado, Boulder, Boulder, CO 80203, USA.
Kelly D SullivanLinda Crnic Institute for Down Syndrome, University of Colorado Anschutz Medical Campus, Aurora, CO 80045, USA; Department of Pharmacology, University of Colorado Anschutz Medical Campus, Aurora, CO 80045, USA; Department of Molecular, Cellular and Developmental Biology, University of Colorado, Boulder, Boulder, CO 80203, USA.
Alessandro QuattroneDepartment of Cellular, Computational and Integrative Biology (CIBIO), University of Trento, via Sommarive 9, 38123 Trento, Italy.
Joaquín M EspinosaLinda Crnic Institute for Down Syndrome, University of Colorado Anschutz Medical Campus, Aurora, CO 80045, USA; Department of Pharmacology, University of Colorado Anschutz Medical Campus, Aurora, CO 80045, USA; Department of Molecular, Cellular and Developmental Biology, University of Colorado, Boulder, Boulder, CO 80203, USA.
Erik DassiDepartment of Cellular, Computational and Integrative Biology (CIBIO), University of Trento, via Sommarive 9, 38123 Trento, Italy. Electronic address: erik.dassi@unitn.it.
Alberto IngaDepartment of Cellular, Computational and Integrative Biology (CIBIO), University of Trento, via Sommarive 9, 38123 Trento, Italy. Electronic address: alberto.inga@unitn.it.
University of Trento · ITUniversity of Colorado Boulder · USUniversity of Colorado Anschutz Medical Campus · US

Funding

Stress- and Promoter-Specific Mechanisms of Transcritpional Activation by p53R01CA117907 · NCI · UNIVERSITY OF COLORADO DENVER · PI ESPINOSA, JOAQUIN M. · 2006 to 2022
$4.4M
Mechanisms of gene expression control during the cellular response to hypoxiaR01GM120109 · NIGMS · UNIVERSITY OF COLORADO DENVER · PI ESPINOSA, JOAQUIN M. · 2016 to 2019
$1.2M
NCI NIH HHS R01 CA117907NIGMS NIH HHS R01 GM120109
6 · The paper itself

Abstract

Activation of p53 by the small molecule Nutlin can result in a combination of cell cycle arrest and apoptosis. The relative strength of these events is difficult to predict by classical gene expression analysis, leaving uncertainty as to the therapeutic benefits. In this study, we report a translational control mechanism shaping p53-dependent apoptosis. Using polysome profiling, we establish Nutlin-induced apoptosis to associate with the enhanced translation of mRNAs carrying multiple copies of an identified 3' UTR CG-rich motif mediating p53-dependent death (CGPD-motif). We identify PCBP2 and DHX30 as CGPD-motif interactors. We find that in cells undergoing persistent cell cycle arrest in response to Nutlin, CGPD-motif mRNAs are repressed by the PCBP2-dependent binding of DHX30 to the motif. Upon DHX30 depletion in these cells, the translation of CGPD-motif mRNAs increases, and the response to Nutlin shifts toward apoptosis. Instead, DHX30 inducible overexpression in SJSA1 cells leads to decreased translation of CGPD-motif mRNAs.

Indexed as

3' Untranslated RegionsApoptosisBase SequenceCell Cycle CheckpointsCell LineGene Expression RegulationGene SilencingHumansImidazolesNeoplasm ProteinsNucleotide MotifsPhenotypePiperazinesPolyribosomesProtein BindingProtein Biosynthesis3' Untranslated RegionsDHX30 protein, humanImidazolesNeoplasm Proteinsnutlin 1PCBP2 protein, humanPiperazinesRNA-Binding ProteinsRNA HelicasesRNA, Messenger3′ UTRapoptosisDHX30Nutlinp53PCBP2polysomal profilingtranscriptiontranslationtranslatome

Identifiers

PMID32234473
PMCPMC7182397
OpenAlexW3014338272

What OpenQuestion holds

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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.