Evidence map›Paper›PMID 33785447›Full record

ReviewSeminars in cancer biology2022

The complexity of p53-mediated metabolic regulation in tumor suppression.

Yanqing Liu, Wei Gu

Open access · greenAbstract readReview
In one paragraph

Review in Seminars in cancer biology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 171 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
171citing papers in PubMed, 2 pooled it
24.1field-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

171 citing papers in PubMed, 2 syntheses or guidelines pooled it, 239 citations in OpenAlex.

  1. Targeting p53 pathways: mechanisms, structures, and advances in therapy.Signal transduction and targeted therapy · 2023
    Pooled it
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  3. Review
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  6. The Dynamic Alliance of p53 and Metabolism in the Tumor Microenvironment Shapes Tumor Evolution.BioEssays : news and reviews in molecular, cellular and developmental biology · 2026
    Review
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111 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

2 authors at 1 institution in 1 country.

Yanqing LiuInstitute for Cancer Genetics, Herbert Irving Comprehensive Cancer Center, Vagelos College of Physicians & Surgeons, Columbia University, 1130 Nicholas Ave, New York, NY, 10032, USA.
Wei GuInstitute for Cancer Genetics, Herbert Irving Comprehensive Cancer Center, Vagelos College of Physicians & Surgeons, Columbia University, 1130 Nicholas Ave, New York, NY, 10032, USA; Department of Pathology and Cell Biology, Vagelos College of Physicians & Surgeons, Columbia University, 1130 Nicholas Ave, New York, NY, 10032, USA. Electronic address: wg8@cumc.columbia.edu.
Cancer Genetics (United States) · US

Funding

Regulation of p53 acetylation and deacetylation in tumorigenesis.R01CA085533 · NCI · COLUMBIA UNIVERSITY HEALTH SCIENCES · PI GU, WEI · 2000 to 2021
$5.2M
Novel small molecule USP7 Inhibitors for p53 activation and cancer therapyR01CA254970 · NCI · COLUMBIA UNIVERSITY HEALTH SCIENCES · PI GU, WEI · 2021 to 2025
$1.8M
Mechanisms of targeting oncoprotein SET in tumor suppressionR01CA216884 · NCI · COLUMBIA UNIVERSITY HEALTH SCIENCES · PI GU, WEI · 2017 to 2021
$1.8M
p53 acetylation in ferroptosis and tumor suppressionR01CA224272 · NCI · COLUMBIA UNIVERSITY HEALTH SCIENCES · PI GU, WEI · 2018 to 2021
$1.5M
NCI NIH HHS R01 CA085533NCI NIH HHS R01 CA216884NCI NIH HHS R01 CA224272NCI NIH HHS R01 CA254970
6 · The paper itself

Abstract

Although the classic activities of p53 including induction of cell-cycle arrest, senescence, and apoptosis are well accepted as critical barriers to cancer development, accumulating evidence suggests that loss of these classic activities is not sufficient to abrogate the tumor suppression activity of p53. Numerous studies suggest that metabolic regulation contributes to tumor suppression, but the mechanisms by which it does so are not completely understood. Cancer cells rewire cellular metabolism to meet the energetic and substrate demands of tumor development. It is well established that p53 suppresses glycolysis and promotes mitochondrial oxidative phosphorylation through a number of downstream targets against the Warburg effect. The role of p53-mediated metabolic regulation in tumor suppression is complexed by its function to promote both cell survival and cell death under different physiological settings. Indeed, p53 can regulate both pro-oxidant and antioxidant target genes for complete opposite effects. In this review, we will summarize the roles of p53 in the regulation of glucose, lipid, amino acid, nucleotide, iron metabolism, and ROS production. We will highlight the mechanisms underlying p53-mediated ferroptosis, AKT/mTOR signaling as well as autophagy and discuss the complexity of p53-metabolic regulation in tumor development.

Indexed as

NeoplasmsTumor Suppressor Protein p53Cell Cycle CheckpointsGlycolysisHumansOxidative PhosphorylationTumor Suppressor Protein p53FerroptosisMetabolismp53Transcriptional activationTumor suppression

Identifiers

PMID33785447
PMCPMC8473587
OpenAlexW3145198654

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.