Evidence map›Paper›PMID 30587523›Full record

ArticleMolecular cancer research : MCR2019

Ovarian Cancer Cells Commonly Exhibit Defective STING Signaling Which Affects Sensitivity to Viral Oncolysis.

Nina Marí Gual Pimenta de Queiroz, Tianli Xia, Hiroyasu Konno, Glen N Barber

Abstract read
In one paragraph

Article in Molecular cancer research : MCR, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 98 papers.

0numbers the graph read from it
0cells of the map it votes in
98citing papers in PubMed
5.3field-weighted citation impact, top 4% 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

98 citing papers in PubMed, 150 citations in OpenAlex.

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  14. cGAS-STING signaling in melanoma: regulation and therapeutic targeting.Naunyn-Schmiedeberg's archives of pharmacology · 2025
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38 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 1 institution in 1 country.

Nina Marí Gual Pimenta de QueirozDepartment of Cell Biology and the Sylvester Comprehensive Cancer Center, University of Miami Miller School of Medicine, Miami, Florida.ORCID 0000-0002-9789-1035
Tianli XiaDepartment of Cell Biology and the Sylvester Comprehensive Cancer Center, University of Miami Miller School of Medicine, Miami, Florida.
Hiroyasu KonnoDepartment of Cell Biology and the Sylvester Comprehensive Cancer Center, University of Miami Miller School of Medicine, Miami, Florida.
Glen N BarberDepartment of Cell Biology and the Sylvester Comprehensive Cancer Center, University of Miami Miller School of Medicine, Miami, Florida. gbarber@med.miami.edu.
Sylvester Comprehensive Cancer Center · US

Funding

Vesicular Stomatitis Virus (VSV) Replication in Malignant CellsR01CA194404 · NCI · UNIVERSITY OF MIAMI SCHOOL OF MEDICINE · PI BARBER, GLEN N. · 2015 to 2019
$1.7M
NCI NIH HHS R01 CA194404
6 · The paper itself

Abstract

Ovarian cancer is the sixth most prevalent cancer in women and the most lethal of the gynecologic malignancies. Treatments have comprised the use of immunotherapeutic agents as well as oncolytic viruses, with varying results for reasons that remain to be clarified. To better understand the mechanisms that may help predict treatment outcome, we have evaluated innate immune signaling in select ovarian cancer cell lines, governed by the Stimulator of Interferon Genes (STING), which controls self or viral DNA-triggered cytokine production. Our results indicate that STING-dependent signaling is habitually defective in majority of ovarian cancer cells examined, frequently through the suppression of STING and/or the cyclic dinucleotide (CDN) enzyme Cyclic GMP-AMP synthase (cGAS) expression, by epigenetic processes. However, STING-independent, dsRNA-activated innate immune cytokine production, which require RIG-I/MDA5, were largely unaffected. Such defects enabled ovarian cancer cells to avoid DNA damage-mediated cytokine production, which would alert the immunosurveillance system. Loss of STING signaling also rendered ovarian cancer cells highly susceptible to viral oncolytic γ34.5 deleted-HSV1 (Herpes simplex virus) infection

Indexed as

AnimalsCell Line, TumorFemaleHumansMembrane ProteinsMiceMice, Inbred BALB CMice, NudeOncolytic VirotherapyOncolytic VirusesOvarian NeoplasmsSignal TransductionSTING ProteinXenograft Model Antitumor AssaysMembrane ProteinsSTING1 protein, humanSTING Protein

Identifiers

PMID30587523
PMCPMC6445711
OpenAlexW2906160139

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.