Evidence map›Paper›PMID 39951185›Full record

ArticleEsophagus : official journal of the Japan Esophageal Society2025

Activation of the tumor cell-intrinsic STING pathway induced by Fusobacterium nucleatum is associated with poor prognosis in esophageal cancer patients.

Shotaro Nakajima, Katsuharu Saito, Satoshi Fukai, Mei Sakuma, Akira Matsuishi, Ryo Kanoda, Yuya Maruyama, Hiroya Suzuki, Hirokazu Okayama, Motonobu Saito and 9 more

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Article in Esophagus : official journal of the Japan Esophageal Society, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing papers in PubMed
–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

4 citing papers in PubMed.

  1. Review
  2. Review
  3. MedComm · 2025
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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

19 authors.

Shotaro NakajimaDepartment of Multidisciplinary Treatment of Cancer and Regional Medical Support, Fukushima Medical University School of Medicine, Fukushima City, Fukushima, 960-1295, Japan. ipsho555@gmail.com.ORCID 0000-0002-9339-3792
Katsuharu SaitoDepartment of Gastrointestinal Tract Surgery, Fukushima Medical University School of Medicine, Fukushima City, Fukushima, 960-1295, Japan.
Satoshi FukaiDepartment of Gastrointestinal Tract Surgery, Fukushima Medical University School of Medicine, Fukushima City, Fukushima, 960-1295, Japan.
Mei SakumaDepartment of Gastrointestinal Tract Surgery, Fukushima Medical University School of Medicine, Fukushima City, Fukushima, 960-1295, Japan.
Akira MatsuishiDepartment of Gastrointestinal Tract Surgery, Fukushima Medical University School of Medicine, Fukushima City, Fukushima, 960-1295, Japan.
Ryo KanodaDepartment of Gastrointestinal Tract Surgery, Fukushima Medical University School of Medicine, Fukushima City, Fukushima, 960-1295, Japan.
Yuya MaruyamaDepartment of Gastrointestinal Tract Surgery, Fukushima Medical University School of Medicine, Fukushima City, Fukushima, 960-1295, Japan.
Hiroya SuzukiDepartment of Gastrointestinal Tract Surgery, Fukushima Medical University School of Medicine, Fukushima City, Fukushima, 960-1295, Japan.
Hirokazu OkayamaDepartment of Gastrointestinal Tract Surgery, Fukushima Medical University School of Medicine, Fukushima City, Fukushima, 960-1295, Japan.
Motonobu SaitoDepartment of Gastrointestinal Tract Surgery, Fukushima Medical University School of Medicine, Fukushima City, Fukushima, 960-1295, Japan.
Kosaku MimuraDepartment of Gastrointestinal Tract Surgery, Fukushima Medical University School of Medicine, Fukushima City, Fukushima, 960-1295, Japan.
Azuma NireiDepartment of Gastrointestinal Tract Surgery, Fukushima Medical University School of Medicine, Fukushima City, Fukushima, 960-1295, Japan.
Tomohiro KikuchiDepartment of Gastrointestinal Tract Surgery, Fukushima Medical University School of Medicine, Fukushima City, Fukushima, 960-1295, Japan.
Hiroyuki HanayamaDepartment of Gastrointestinal Tract Surgery, Fukushima Medical University School of Medicine, Fukushima City, Fukushima, 960-1295, Japan.
Zenichiro SazeDepartment of Gastrointestinal Tract Surgery, Fukushima Medical University School of Medicine, Fukushima City, Fukushima, 960-1295, Japan.
Tomoyuki MommaDepartment of Gastrointestinal Tract Surgery, Fukushima Medical University School of Medicine, Fukushima City, Fukushima, 960-1295, Japan.
Kyoko NishiyamaDepartment of Microbiology, Fukushima Medical University School of Medicine, Fukushima City, Fukushima, Japan.
Tatsuo SuzutaniDepartment of Microbiology, Fukushima Medical University School of Medicine, Fukushima City, Fukushima, Japan.
Koji KonoDepartment of Multidisciplinary Treatment of Cancer and Regional Medical Support, Fukushima Medical University School of Medicine, Fukushima City, Fukushima, 960-1295, Japan. kojikono@fmu.ac.jp.

Funding

Japan Society for the Promotion of Science 22K08779
6 · The paper itself

Abstract

backgroundIntratumoral Fusobacterium nucleatum (Fn) infection is closely associated with poor prognosis in esophageal cancer (EC) due to its impact on the tumor microenvironment (TME). The tumor cell-intrinsic cyclic GMP-AMP synthase (cGAS)-stimulator of interferon genes (STING) pathway is critical for regulating immune cell activation in the TME. However, the link between intratumoral Fn infection and the activation of the cGAS-STING pathway in tumor cells, as well as its effects on EC progression, remains largely unknown.

methodsIn the present study, we investigated the impact of intratumoral Fn infection on the activation of the tumor cell-intrinsic cGAS-STING pathway and EC progression by analyzing our own EC cohort and performing in vitro experiments using co-cultures of EC-cell lines and Fn.

resultsThe expression of tumor cell-intrinsic STING was significantly associated with worse prognosis in Fn-high EC patients. Exposure to Fn significantly activated the STING pathway in EC cells. RNA-seq analysis revealed that exposure to Fn markedly activated cytokine-chemokine-related signaling pathways and induced the expression of several cytokines and chemokines in STING-expressing EC cells. Among the differentially expressed cytokine and chemokine genes in EC cells co-cultured with Fn, analysis of TCGA datasets demonstrated that the expression of CCL20, CXCL10, and CSF2 may be associated with poor prognosis in EC patients.

conclusionWe revealed that the activation of the STING signaling pathway and the subsequent expression of cytokines and chemokines in EC cells induced by Fn infection may be closely associated with poor prognosis in EC patients.

Indexed as

Esophageal NeoplasmsFusobacterium InfectionsFusobacterium nucleatumMembrane ProteinsAgedCell Line, TumorCoculture TechniquesCyclic Guanosine Monophosphate-Adenosine Monophosphate SynthaseCytokinesFemaleHumansMaleMiddle AgedNucleotidyltransferasesPrognosisSignal TransductioncGAS protein, humanCyclic Guanosine Monophosphate-Adenosine Monophosphate SynthaseCytokinesMembrane ProteinsNucleotidyltransferasesSTING1 protein, humanSTING ProteinEsophageal cancerFusobacterium nucleatumTumor cell-intrinsic STING pathwayTumor microenvironment

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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.