Evidence map›Paper›PMID 31799772›Full record

ReviewCancer science2020

Cellular senescence and senescence-associated secretory phenotype via the cGAS-STING signaling pathway in cancer.

Tze Mun Loo, Kenichi Miyata, Yoko Tanaka, Akiko Takahashi

Open access · goldAbstract readReview
In one paragraph

Review in Cancer science, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 145 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
145citing papers in PubMed, 2 pooled it
6.6field-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

145 citing papers in PubMed, 2 syntheses or guidelines pooled it, 210 citations in OpenAlex.

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  9. [Mechanisms of cGAS-STING-mediated chronic inflammation and targeted interventions in brain aging].Zhejiang da xue xue bao. Yi xue ban = Journal of Zhejiang University. Medical sciences · 2026
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85 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

4 authors at 2 institutions in 1 country.

Tze Mun LooProject for Cellular Senescence, The Cancer Institute, Japanese Foundation for Cancer Research, Tokyo, Japan.
Kenichi MiyataProject for Cellular Senescence, The Cancer Institute, Japanese Foundation for Cancer Research, Tokyo, Japan.
Yoko TanakaProject for Cellular Senescence, The Cancer Institute, Japanese Foundation for Cancer Research, Tokyo, Japan.
Akiko TakahashiProject for Cellular Senescence, The Cancer Institute, Japanese Foundation for Cancer Research, Tokyo, Japan.ORCID https://orcid.org/0000-0003-1904-7645
Japanese Foundation For Cancer Research · JPJapan Agency for Medical Research and Development · JP

Funding

Japan Agency for Medical Research and Development PRIME/19gm6110023h0001Japan Science and Technology Agency PRESTO/JPMJPR17H7Japan Society for the Promotion of Science 18K15073Japan Society for the Promotion of Science 18K15254Japan Society for the Promotion of Science 19H03507Japan Society for the Promotion of Science 19J00796Princess Takamatsu Cancer Research FundTakeda Science Foundationthe Vehicle Racing Commemorative Foundation
6 · The paper itself

Abstract

Cellular senescence is historically regarded as a tumor suppression mechanism to prevent damaged cells from aberrant proliferation in benign and premalignant tumors. However, recent findings have suggested that senescent cells contribute to tumorigenesis and age-associated pathologies through the senescence-associated secretory phenotype (SASP). Therefore, to control age-associated cancer, it is important to understand the molecular mechanisms of the SASP in the cancer microenvironment. New findings have suggested that the cyclic GMP-AMP synthase (cGAS)-stimulator of interferon genes (STING) signaling pathway, a critical indicator of innate immune response, triggers the SASP in response to accumulation of cytoplasmic DNA (cytoplasmic chromatin fragments, mtDNA and cDNA) in senescent cells. Notably, the cGAS-STING signaling pathway promotes or inhibits tumorigenesis depending on the biological context in vivo, indicating that it may be a potential therapeutic target for cancer. Herein, we review the regulatory machinery and biological function of the SASP via the cGAS-STING signaling pathway in cancer.

Indexed as

Signal TransductionCellular SenescenceCyclic Guanosine Monophosphate-Adenosine Monophosphate SynthaseCytoplasmDNA DamageGene Expression Regulation, NeoplasticHumansImmunity, InnateMembrane ProteinsNeoplasmsNucleotidyltransferasesPhenotypeSTING ProteinTumor MicroenvironmentcGAS protein, humanCyclic Guanosine Monophosphate-Adenosine Monophosphate SynthaseMembrane ProteinsNucleotidyltransferasesSTING1 protein, humanSTING Proteincellular senescencecGAS-STINGDNA damageSASPtumorigenesis

Identifiers

PMID31799772
PMCPMC7004529
OpenAlexW2991832873

What OpenQuestion holds

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LicenceCC BY-NC
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.