Evidence map›Paper›PMID 39986611›Full record

ReviewMolecules and cells2025

Metabolic regulation by p53: Implications for cancer therapy.

Ki Yeon Koo, Kwanho Moon, Hwa Seob Song, Min-Sik Lee

Abstract readReview
In one paragraph

Review in Molecules and cells, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.

0numbers the graph read from it
0cells of the map it votes in
26citing papers in PubMed
–field-weighted citation impact
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

26 citing papers in PubMed.

  1. Revisiting tumor immunogenicity through the lens of mutant p53: Implications for cancer immunotherapy.Apoptosis : an international journal on programmed cell death · 2026
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  2. 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
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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

4 authors.

Ki Yeon KooDepartment of Life Sciences, POSTECH, Pohang, Korea.
Kwanho MoonDepartment of Life Sciences, POSTECH, Pohang, Korea.
Hwa Seob SongDepartment of Life Sciences, POSTECH, Pohang, Korea.
Min-Sik LeeDepartment of Life Sciences, POSTECH, Pohang, Korea. Electronic address: minsiklee@postech.ac.kr.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The tumor suppressor p53, long known for its roles in maintaining genomic integrity and suppressing tumorigenesis, has recently been recognized as a key regulator of cellular metabolism. Here, we review p53's emerging metabolic functions, highlighting its ability to orchestrate glucose, amino acid, and lipid metabolism. By promoting oxidative phosphorylation while inhibiting glycolysis and anabolic pathways, wild-type p53 counters metabolic reprogramming characteristic of cancer cells, such as the Warburg effect, and protects cells from mild cellular stresses. In contrast, mutant p53 disrupts these processes, fostering metabolic adaptations that support tumor progression. These findings pave the way for therapeutic approaches targeting p53-driven metabolic vulnerabilities in cancer.

Indexed as

NeoplasmsTumor Suppressor Protein p53AnimalsGlucoseGlycolysisHumansLipid MetabolismOxidative PhosphorylationGlucoseTumor Suppressor Protein p53Cancer metabolismMetabolic reprogrammingP53 (TP53)Tumor suppressor

Identifiers

PMID39986611
PMCPMC11925517

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.