Evidence map›Paper›PMID 32886745›Full record

ArticleThe Journal of cell biology2020

p53 deficiency triggers dysregulation of diverse cellular processes in physiological oxygen.

Liz J Valente, Amy Tarangelo, Albert Mao Li, Marwan Naciri, Nitin Raj, Anthony M Boutelle, Yang Li, Stephano Spano Mello, Kathryn Bieging-Rolett, Ralph J DeBerardinis and 3 more

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of cell biology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
2.0field-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

20 citing papers in PubMed, 40 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Article
  5. The cell biology of ferroptosis.Nature reviews. Molecular cell biology · 2024
    Review
  6. The TP53-activated E3 ligase RNF144B is a tumour suppressor that prevents genomic instability.Journal of experimental & clinical cancer research : CR · 2024
    Article
  7. Article
  8. Review
  9. Article
  10. Multifaceted role for p53 in pancreatic cancer suppression.Proceedings of the National Academy of Sciences of the United States of America · 2023
    Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. Review
  19. Article
  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

13 authors at 4 institutions in 2 countries.

Liz J ValenteDivision of Radiation and Cancer Biology, Department of Radiation Oncology, Stanford University School of Medicine, Stanford, CA.
Amy TarangeloDepartment of Biology, Stanford University, Stanford, CA.
Albert Mao LiDivision of Radiation and Cancer Biology, Department of Radiation Oncology, Stanford University School of Medicine, Stanford, CA.
Marwan NaciriDivision of Radiation and Cancer Biology, Department of Radiation Oncology, Stanford University School of Medicine, Stanford, CA.
Nitin RajDivision of Radiation and Cancer Biology, Department of Radiation Oncology, Stanford University School of Medicine, Stanford, CA.
Anthony M BoutelleDivision of Radiation and Cancer Biology, Department of Radiation Oncology, Stanford University School of Medicine, Stanford, CA.
Yang LiDivision of Radiation and Cancer Biology, Department of Radiation Oncology, Stanford University School of Medicine, Stanford, CA.
Stephano Spano MelloDivision of Radiation and Cancer Biology, Department of Radiation Oncology, Stanford University School of Medicine, Stanford, CA.
Kathryn Bieging-RolettDivision of Radiation and Cancer Biology, Department of Radiation Oncology, Stanford University School of Medicine, Stanford, CA.
Ralph J DeBerardinisChildren's Medical Center Research Institute, University of Texas Southwestern Medical Center, Dallas, TX.
Jiangbin YeDivision of Radiation and Cancer Biology, Department of Radiation Oncology, Stanford University School of Medicine, Stanford, CA.
Scott J DixonDepartment of Biology, Stanford University, Stanford, CA.
Laura D AttardiDivision of Radiation and Cancer Biology, Department of Radiation Oncology, Stanford University School of Medicine, Stanford, CA.
Stanford University · USChildren's Medical Center · USUniversité Claude Bernard Lyon 1 · FRUniversity of Rochester Medical Center · US

Funding

Leveraging innovative technologies in basic and clinical cancer researchT32CA009302 · NCI · STANFORD UNIVERSITY · PI LAURA D ATTARDI, Aaron M Newman · 1985 to 2026
$19.1M
Integrative approaches to elucidate p53 transcriptional networks during carcinogenesisR35CA197591 · NCI · STANFORD UNIVERSITY · PI LAURA D ATTARDI · 2015 to 2026
$11.6M
Metabolic Regulators of Tumor Growth and ProgressionR35CA220449 · NCI · UT SOUTHWESTERN MEDICAL CENTER · PI RALPH J DEBERARDINIS · 2017 to 2026
$9.4M
Characterizing the Regulation of FerroptosisR01GM122923 · NIGMS · STANFORD UNIVERSITY · PI Scott Dixon · 2017 to 2026
$3.4M
NCI NIH HHS R35 CA197591NCI NIH HHS R35 CA220449NCI NIH HHS T32 CA009302NIGMS NIH HHS R01 GM122923
6 · The paper itself

Abstract

The mechanisms by which TP53, the most frequently mutated gene in human cancer, suppresses tumorigenesis remain unclear. p53 modulates various cellular processes, such as apoptosis and proliferation, which has led to distinct cellular mechanisms being proposed for p53-mediated tumor suppression in different contexts. Here, we asked whether during tumor suppression p53 might instead regulate a wide range of cellular processes. Analysis of mouse and human oncogene-expressing wild-type and p53-deficient cells in physiological oxygen conditions revealed that p53 loss concurrently impacts numerous distinct cellular processes, including apoptosis, genome stabilization, DNA repair, metabolism, migration, and invasion. Notably, some phenotypes were uncovered only in physiological oxygen. Transcriptomic analysis in this setting highlighted underappreciated functions modulated by p53, including actin dynamics. Collectively, these results suggest that p53 simultaneously governs diverse cellular processes during transformation suppression, an aspect of p53 function that would provide a clear rationale for its frequent inactivation in human cancer.

Indexed as

ApoptosisCellular SenescenceDNA RepairAnimalsCell Transformation, NeoplasticFemaleFibroblastsMetabolomeMiceMutationOxygenSignal TransductionTumor Suppressor Protein p53OxygenTrp53 protein, mouseTumor Suppressor Protein p53

Identifiers

PMID32886745
PMCPMC7594498
OpenAlexW3083387679

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-SA
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.