Evidence map›Paper›PMID 27698118›Full record

ArticleProceedings of the National Academy of Sciences of the United States of America2016

Activation of SAT1 engages polyamine metabolism with p53-mediated ferroptotic responses.

Yang Ou, Shang-Jui Wang, Dawei Li, Bo Chu, Wei Gu

Open access · bronzeAbstract read
In one paragraph

Article in Proceedings of the National Academy of Sciences of the United States of America, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 552 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
552citing papers in PubMed, 1 pooled it
10.6field-weighted citation impact, top 1% 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

552 citing papers in PubMed, 1 synthesis or guideline pooled it, 738 citations in OpenAlex.

  1. Pooled it
  2. Review
  3. Ferroptosis in health and disease.Molecular biomedicine · 2026
    Review
  4. Article
  5. Article
  6. Article
  7. High-Density Type I Collagen Promotes IFN-γAdvanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026
    Article
  8. Article
  9. Article
  10. Review
  11. Review
  12. Article
  13. Review
  14. Article
  15. Article
  16. Review
  17. Review
  18. Review
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  20. Article

492 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

5 authors at 1 institution in 1 country.

Yang OuInstitute for Cancer Genetics, Department of Pathology and Cell Biology, College of Physicians and Surgeons, Columbia University, New York, NY 10032.
Shang-Jui WangInstitute for Cancer Genetics, Department of Pathology and Cell Biology, College of Physicians and Surgeons, Columbia University, New York, NY 10032.
Dawei LiInstitute for Cancer Genetics, Department of Pathology and Cell Biology, College of Physicians and Surgeons, Columbia University, New York, NY 10032.
Bo ChuInstitute for Cancer Genetics, Department of Pathology and Cell Biology, College of Physicians and Surgeons, Columbia University, New York, NY 10032.
Wei GuInstitute for Cancer Genetics, Department of Pathology and Cell Biology, College of Physicians and Surgeons, Columbia University, New York, NY 10032; wg8@cumc.columbia.edu.
Cancer Genetics (United States) · US

Funding

PW1--A mediator of cell survival by NFKB and cell death by p53P01CA080058 · NCI · MOUNT SINAI SCHOOL OF MEDICINE OF NYU · PI AARONSON, STUART A · 2000 to 2016
$20.2M
CELL, MOLECULAR AND DEVELOPMENTAL BIOLOGY OF CANCERT32CA009503 · NCI · COLUMBIA UNIV NEW YORK MORNINGSIDE · PI GAUTIER, JEAN · 1985 to 2016
$6.8M
Regulation of p53 acetylation and deacetylation in tumorigenesis.R01CA085533 · NCI · COLUMBIA UNIVERSITY HEALTH SCIENCES · PI GU, WEI · 2000 to 2021
$5.2M
Regulation of SLC7A11 by p53 in cancer metabolismR01CA190477 · NCI · COLUMBIA UNIVERSITY HEALTH SCIENCES · PI GU, WEI · 2016 to 2020
$1.8M
Role of p53-mediated unconventional functions in tumor suppressionR01CA172023 · NCI · COLUMBIA UNIVERSITY HEALTH SCIENCES · PI GU, WEI · 2012 to 2016
$1.6M
NCI NIH HHS P01 CA080058NCI NIH HHS R01 CA085533NCI NIH HHS R01 CA172023NCI NIH HHS R01 CA190477NCI NIH HHS T32 CA009503
6 · The paper itself

Abstract

Although p53-mediated cell-cycle arrest, senescence, and apoptosis remain critical barriers to cancer development, the emerging role of p53 in cell metabolism, oxidative responses, and ferroptotic cell death has been a topic of great interest. Nevertheless, it is unclear how p53 orchestrates its activities in multiple metabolic pathways into tumor suppressive effects. Here, we identified the SAT1 (spermidine/spermine N

Indexed as

AcetyltransferasesAnimalsApoptosisArachidonate 15-LipoxygenaseCarcinogenesisCell Cycle CheckpointsCell DeathCell Line, TumorCRISPR-Cas SystemsDiamine N-AcetyltransferaseGene Expression Regulation, NeoplasticGene Knockdown TechniquesHumansLipid PeroxidationMetabolic Networks and PathwaysMiceAcetyltransferasesALOX15 protein, humanArachidonate 15-LipoxygenaseDiamine N-AcetyltransferaseMDM2 protein, humanNeoplasm ProteinsPolyaminesProto-Oncogene Proteins c-mdm2Reactive Oxygen SpeciesSpermidineSpermineSTUB1 protein, humanTumor Suppressor Protein p53Ubiquitin-Protein Ligasesferroptosisp53polyamine metabolismSAT1tumor suppression

Identifiers

PMID27698118
PMCPMC5098629
OpenAlexW2527907612

What OpenQuestion holds

Textmetadata
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.