Evidence map›Paper›PMID 37282604›Full record

ArticleGut microbes

Gut microbiota dysbiosis promotes the development of epithelial ovarian cancer

Xinyue Hu, Xuan Xu, Xiangdi Zeng, Rui Jin, Shengnan Wang, Huifu Jiang, Yuwen Tang, Guanxiang Chen, Jing Wei, Tingtao Chen and 1 more

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Gut microbes. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 42 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
42citing papers in PubMed, 1 pooled it
8.6field-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

42 citing papers in PubMed, 1 synthesis or guideline pooled it, 52 citations in OpenAlex.

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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

11 authors at 1 institution in 1 country.

Xinyue HuDepartment of Obstetrics and Gynecology, The Second Affiliated Hospital of Nanchang University, Nanchang, China.
Xuan XuNational Engineering Research Center for Bioengineering Drugs and the Technologies, Institute of Translational Medicine, Nanchang University, Nanchang, China.
Xiangdi ZengNational Engineering Research Center for Bioengineering Drugs and the Technologies, Institute of Translational Medicine, Nanchang University, Nanchang, China.
Rui JinNational Engineering Research Center for Bioengineering Drugs and the Technologies, Institute of Translational Medicine, Nanchang University, Nanchang, China.
Shengnan WangDepartment of Obstetrics and Gynecology, The Second Affiliated Hospital of Nanchang University, Nanchang, China.
Huifu JiangDepartment of Obstetrics and Gynecology, The Second Affiliated Hospital of Nanchang University, Nanchang, China.
Yuwen TangDepartment of Obstetrics and Gynecology, The Second Affiliated Hospital of Nanchang University, Nanchang, China.
Guanxiang ChenDepartment of Obstetrics and Gynecology, The Second Affiliated Hospital of Nanchang University, Nanchang, China.
Jing WeiNational Engineering Research Center for Bioengineering Drugs and the Technologies, Institute of Translational Medicine, Nanchang University, Nanchang, China.
Tingtao ChenNational Engineering Research Center for Bioengineering Drugs and the Technologies, Institute of Translational Medicine, Nanchang University, Nanchang, China.ORCID 0000-0002-0506-8536
Qi ChenDepartment of Obstetrics and Gynecology, The Second Affiliated Hospital of Nanchang University, Nanchang, China.
Nanchang University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Epithelial ovarian cancer (EOC) is the most lethal gynecological cancer, which remains a threat to female health at all ages. Hypotheses for EOC development include the continuous presence of inflammation, in which microbiota and inflammatory cytokines participate in cancer-related signaling pathway activation. Hedgehog (Hh) signaling is prominent for EOC progression, and interacts with inflammation response related to gut microbiota (GM). However, the precise roles of GM during this process are unknown. Here, we showed that the GM from patients with EOC differed from that of healthy women and had GM dysbiosis. We found that EOC modeling may lead to GM changes in mice, and it restored after the administration of GM from healthy controls, while GM from patients with EOC further exacerbated GM dysbiosis. Furthermore, we found that GM from EOC markedly promoted tumor progression and activated Hh signaling; meanwhile, it increased the extent of inflammation and activated NF-κB signaling, but GM from healthy controls improved them. Our results demonstrate how GM dysbiosis promoted EOC progression by activating Hh signaling mediated by TLR4/NF-κB signaling. We anticipate our assay to be a new thought for exploring the role of GM in EOC development. Furthermore, improving GM dysbiosis is a novel therapeutic approach for delaying EOC development.

Indexed as

Gastrointestinal MicrobiomeOvarian NeoplasmsAnimalsCarcinoma, Ovarian EpithelialCell Line, TumorDysbiosisFemaleHedgehog ProteinsHumansInflammationMiceNF-kappa BSignal TransductionHedgehog ProteinsNF-kappa Bcancer progressionEpithelial ovarian cancergut microbiotaHedgehog signaling pathwayNF-κB signaling pathway

Identifiers

PMID37282604
PMCPMC10249449
OpenAlexW4379598727

What OpenQuestion holds

Textmetadata
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.