Evidence map›Paper›PMID 28985506›Full record

ArticleMolecular cell2017

NRF2 Is a Major Target of ARF in p53-Independent Tumor Suppression.

Delin Chen, Omid Tavana, Bo Chu, Luke Erber, Yue Chen, Richard Baer, Wei Gu

Open access · bronzeAbstract read
In one paragraph

Article in Molecular cell, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 214 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
214citing papers in PubMed, 2 pooled it
7.1field-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

214 citing papers in PubMed, 2 syntheses or guidelines pooled it, 309 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Significance of GSH and HRedox report : communications in free radical research · 2026
    Review
  4. Article
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  6. Ferroptosis as a target mechanism in heart and kidney disease.The Journal of clinical investigation · 2026
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  20. [Bioinformatics screening and analysis of key genes of ferroptosis and autophagy in alcoholic liver disease and their validation].Zhonghua gan zang bing za zhi = Zhonghua ganzangbing zazhi = Chinese journal of hepatology · 2025
    Article

154 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

7 authors at 3 institutions in 1 country.

Delin ChenInstitute for Cancer Genetics, Department of Pathology and Cell Biology, College of Physicians and Surgeons, Columbia University, 1130 St. Nicholas Avenue, New York, NY 10032, USA; Herbert Irving Comprehensive Cancer Center, College of Physicians and Surgeons, Columbia University, 1130 St. Nicholas Avenue, New York, NY 10032, USA.
Omid TavanaInstitute for Cancer Genetics, Department of Pathology and Cell Biology, College of Physicians and Surgeons, Columbia University, 1130 St. Nicholas Avenue, New York, NY 10032, USA; Herbert Irving Comprehensive Cancer Center, College of Physicians and Surgeons, Columbia University, 1130 St. Nicholas Avenue, New York, NY 10032, USA.
Bo ChuInstitute for Cancer Genetics, Department of Pathology and Cell Biology, College of Physicians and Surgeons, Columbia University, 1130 St. Nicholas Avenue, New York, NY 10032, USA; Herbert Irving Comprehensive Cancer Center, College of Physicians and Surgeons, Columbia University, 1130 St. Nicholas Avenue, New York, NY 10032, USA.
Luke ErberDepartments of Biochemistry, Molecular Biology, and Biophysics, University of Minnesota, Minneapolis, MN 55455, USA.
Yue ChenDepartments of Biochemistry, Molecular Biology, and Biophysics, University of Minnesota, Minneapolis, MN 55455, USA.
Richard BaerInstitute for Cancer Genetics, Department of Pathology and Cell Biology, College of Physicians and Surgeons, Columbia University, 1130 St. Nicholas Avenue, New York, NY 10032, USA; Herbert Irving Comprehensive Cancer Center, College of Physicians and Surgeons, Columbia University, 1130 St. Nicholas Avenue, New York, NY 10032, USA.
Wei GuInstitute for Cancer Genetics, Department of Pathology and Cell Biology, College of Physicians and Surgeons, Columbia University, 1130 St. Nicholas Avenue, New York, NY 10032, USA; Herbert Irving Comprehensive Cancer Center, College of Physicians and Surgeons, Columbia University, 1130 St. Nicholas Avenue, New York, NY 10032, USA. Electronic address: wg8@cumc.columbia.edu.
Cancer Genetics (United States) · USUniversity of Minnesota · USColumbia University · US

Funding

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
Mechanisms of targeting oncoprotein SET in tumor suppressionR01CA216884 · NCI · COLUMBIA UNIVERSITY HEALTH SCIENCES · PI GU, WEI · 2017 to 2021
$1.8M
The BARD1 tumor suppressor and breast cancerR01CA172272 · NCI · COLUMBIA UNIVERSITY HEALTH SCIENCES · PI BAER, RICHARD J · 2013 to 2017
$1.7M
Mechanisms of novel cancer targets in ARF-mediated tumor suppressionR01CA169246 · NCI · COLUMBIA UNIVERSITY HEALTH SCIENCES · PI GU, WEI · 2012 to 2016
$1.6M
NCI NIH HHS R01 CA085533NCI NIH HHS R01 CA169246NCI NIH HHS R01 CA172272NCI NIH HHS R01 CA190477NCI NIH HHS R01 CA216884
6 · The paper itself

Abstract

Although ARF can suppress tumor growth by activating p53 function, the mechanisms by which it suppresses tumor growth independently of p53 are not well understood. Here, we identified ARF as a key regulator of nuclear factor E2-related factor 2 (NRF2) through complex purification. ARF inhibits the ability of NRF2 to transcriptionally activate its target genes, including SLC7A11, a component of the cystine/glutamate antiporter that regulates reactive oxygen species (ROS)-induced ferroptosis. As a consequence, ARF expression sensitizes cells to ferroptosis in a p53-independent manner while ARF depletion induces NRF2 activation and promotes cancer cell survival in response to oxidative stress. Moreover, the ability of ARF to induce p53-independent tumor growth suppression in mouse xenograft models is significantly abrogated upon NRF2 overexpression. These results demonstrate that NRF2 is a major target of p53-independent tumor suppression by ARF and also suggest that the ARF-NRF2 interaction acts as a new checkpoint for oxidative stress responses.

Indexed as

Gene Expression Regulation, NeoplasticAmino Acid Transport System y+AnimalsBone NeoplasmsCell Line, TumorCyclin-Dependent Kinase Inhibitor p16Cyclin-Dependent Kinase Inhibitor p18Epithelial CellsFibroblastsHEK293 CellsHeterograftsHumansMiceMice, NudeNF-E2-Related Factor 2OsteoblastsAmino Acid Transport System y+CDKN2A protein, humanCyclin-Dependent Kinase Inhibitor p16Cyclin-Dependent Kinase Inhibitor p18NFE2L2 protein, humanNF-E2-Related Factor 2Reactive Oxygen SpeciesSLC7A11 protein, humanTumor Suppressor Protein p53ARFferroptosisNRF2oxidative stressp53ROStranscriptional regulation

Identifiers

PMID28985506
PMCPMC5683418
OpenAlexW2761645877

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.