Evidence map›Paper›PMID 40640925›Full record

ReviewJournal of translational medicine2025

The cGAS-STING pathway: a dual regulator of immune response in cancer and therapeutic implications.

Zhanghao Huang, Jun Zhu, You Lang Zhou, Jiahai Shi

Abstract readReview
In one paragraph

Review in Journal of translational medicine, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
32citing papers in PubMed, 1 pooled it
–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

32 citing papers in PubMed, 1 synthesis or guideline pooled it.

  1. Pooled it
  2. Review
  3. Review
  4. Article
  5. Review
  6. Therapeutic targeting of the cGAS-STING pathway in human disease.The Journal of clinical investigation · 2026
    Review
  7. Review
  8. Review
  9. Interstitial lung disease and the STING pathway.The Journal of clinical investigation · 2026
    Review
  10. Review
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  12. Review
  13. Review
  14. ROS-Responsive MnOJournal of nanobiotechnology · 2026
    Article
  15. cGAS-STING signaling in pollution-induced toxicity: mechanism and relieving medication.Apoptosis : an international journal on programmed cell death · 2026
    Review
  16. Article
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  18. Review
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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.

Zhanghao HuangMedical School of Nantong University, Nantong University, Nantong, 226001, China.
Jun ZhuDepartment of Thoracic Surgery, Affiliated Hospital of Nantong University, NantongJiangsu, 226001, China.
You Lang ZhouMedical School of Nantong University, Nantong University, Nantong, 226001, China.
Jiahai ShiDepartment of Thoracic Surgery, Affiliated Hospital of Nantong University, NantongJiangsu, 226001, China. sjh@ntu.edu.cn.ORCID 0000-0002-8635-5376

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

While the cyclic GMP-AMP synthase (cGAS)-stimulator of interferon genes (STING) pathway promotes anti-tumor immunity by detecting cytoplasmic DNA and inducing type I interferons, it also facilitates immune evasion through PD-L1 upregulation. Autophagy enhances cGAS signaling by delivering it to autophagosomes, boosting DNA sensing, while phase separation into liquid droplets further amplifies its activity and regulates autophagy, affecting tumor proliferation. Oxidative stress and DNA damage activate cGAS-STING, triggering pro-inflammatory cytokines that drive chronic inflammation and metabolic disorders. Interactions with immune checkpoint inhibitors augment T cell responses against tumors, yet concurrent PD-L1 induction underscores a complex balance between activation and suppression. Therapeutic strategies-combining DNA damage response inhibitors with checkpoint blockade-show promise in amplifying antitumor immunity. Moreover, post-translational modifications, including m6A methylation and acetylation, fine-tune cGAS function and downstream signaling. Together, these insights reveal the dualistic nature of cGAS-STING in cancer, offering avenues for targeted interventions that leverage its immunostimulatory potential while mitigating mechanisms of immune escape. Additionally, cGAS-driven inflammation links to metabolic dysfunction and chronic disease, underscoring its broad clinical relevance.

Indexed as

ImmunityMembrane ProteinsNeoplasmsNucleotidyltransferasesSignal TransductionAnimalsAutophagyCyclic Guanosine Monophosphate-Adenosine Monophosphate SynthaseHumansSTING ProteincGAS protein, humanCyclic Guanosine Monophosphate-Adenosine Monophosphate SynthaseMembrane ProteinsNucleotidyltransferasesSTING1 protein, humanSTING ProteinAutophagycGAS-STING pathwayImmune responseTherapeutic strategiesTumor evasion

Identifiers

PMID40640925
PMCPMC12247247

What OpenQuestion holds

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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.