Evidence map›Paper›PMID 36638783›Full record

ArticleMolecular cell2023

p53 engages the cGAS/STING cytosolic DNA sensing pathway for tumor suppression.

Monisankar Ghosh, Suchandrima Saha, Jinyu Li, David C Montrose, Luis A Martinez

Open access · bronzeAbstract read
In one paragraph

Article in Molecular cell, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 112 papers.

0numbers the graph read from it
0cells of the map it votes in
112citing papers in PubMed
23.5field-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

112 citing papers in PubMed, 143 citations in OpenAlex.

  1. Review
  2. Revisiting tumor immunogenicity through the lens of mutant p53: Implications for cancer immunotherapy.Apoptosis : an international journal on programmed cell death · 2026
    Review
  3. Article
  4. Article
  5. Review
  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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52 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

5 authors at 1 institution in 1 country.

Monisankar GhoshDepartment of Pathology, Renaissance School of Medicine, Stony Brook University, Stony Brook, NY 11790, USA; Stony Brook Cancer Center, Stony Brook, NY 11790, USA.
Suchandrima SahaDepartment of Pathology, Renaissance School of Medicine, Stony Brook University, Stony Brook, NY 11790, USA; Stony Brook Cancer Center, Stony Brook, NY 11790, USA.
Jinyu LiDepartment of Pathology, Renaissance School of Medicine, Stony Brook University, Stony Brook, NY 11790, USA; Stony Brook Cancer Center, Stony Brook, NY 11790, USA.
David C MontroseDepartment of Pathology, Renaissance School of Medicine, Stony Brook University, Stony Brook, NY 11790, USA; Stony Brook Cancer Center, Stony Brook, NY 11790, USA.
Luis A MartinezDepartment of Pathology, Renaissance School of Medicine, Stony Brook University, Stony Brook, NY 11790, USA; Stony Brook Cancer Center, Stony Brook, NY 11790, USA. Electronic address: luis.martinez@stonybrookmedicine.edu.
Stony Brook School · US

Funding

Transcriptional Regulations of Oncongenic Properties of Mutant P53R01CA166974 · NCI · UNIVERSITY OF MISSISSIPPI MED CTR · PI Luis Alfonso Martinez · 2013 to 2026
$3.3M
Reducing serine biosynthesis and utilization as a novel approach for colon cancer preventionK22CA226033 · NCI · STATE UNIVERSITY NEW YORK STONY BROOK · PI MONTROSE, DAVID C · 2019 to 2021
$688k
NCI NIH HHS K22 CA226033NCI NIH HHS R01 CA166974
6 · The paper itself

Abstract

Tumor suppression by TP53 involves cell-autonomous and non-cell-autonomous mechanisms. TP53 can suppress tumor growth by modulating immune system functions; however, the mechanistic basis for this activity is not well understood. We report that p53 promotes the degradation of the DNA exonuclease TREX1, resulting in cytosolic dsDNA accumulation. We demonstrate that p53 requires the ubiquitin ligase TRIM24 to induce TREX1 degradation. The cytosolic DNA accumulation resulting from TREX1 degradation activates the cytosolic DNA-sensing cGAS/STING pathway, resulting in induction of type I interferons. TREX1 overexpression sufficed to block p53 activation of the cGAS/STING pathway. p53-mediated induction of type I interferon (IFNB1) is suppressed by cGAS/STING knockout, and p53's tumor suppressor activities are compromised by the loss of signaling through the cGAS/STING pathway. Thus, our study reveals that p53 utilizes the cGAS/STING innate immune system pathway for both cell-intrinsic and cell-extrinsic tumor suppressor activities.

Indexed as

Immunity, InnateInterferon Type IDNAMembrane ProteinsNucleotidyltransferasesSignal TransductionSTING ProteinTumor Suppressor Protein p53DNAInterferon Type IMembrane ProteinsNucleotidyltransferasesSTING1 protein, humanSTING ProteinTumor Suppressor Protein p53cGASinnate immunityp53STINGTREX1tumor suppression

Identifiers

PMID36638783
PMCPMC9993620
OpenAlexW4315705275

What OpenQuestion holds

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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.