Evidence map›Paper›PMID 38481347›Full record

ArticleBiomarker research2024

STAT3-mediated up-regulation of DAB2 via SRC-YAP1 signaling axis promotes Helicobacter pylori-driven gastric tumorigenesis.

Yantao Duan, Pengfei Kong, Mingzhu Huang, Yonghao Yan, Yi Dou, Binhao Huang, Jing Guo, Wei Kang, Caixia Zhu, Yuyan Wang and 3 more

Open access · goldAbstract read
In one paragraph

Article in Biomarker research, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.

0numbers the graph read from it
0cells of the map it votes in
9citing papers in PubMed
2.3field-weighted citation impact, top 14% 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

9 citing papers in PubMed, 7 citations in OpenAlex.

  1. Review
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  3. Advances inOncology letters · 2026
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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

13 authors at 3 institutions in 1 country.

Yantao Duan *Department of Gastric Surgery, Fudan University Shanghai Cancer Center, Shanghai, 200032, China.
Pengfei Kong *Department of Gastric Surgery, Fudan University Shanghai Cancer Center, Shanghai, 200032, China.
Mingzhu Huang *Department of Oncology, Shanghai Medical College, Fudan University, Shanghai, 200032, China. mingzhuhuang0718@163.com.
Yonghao Yan *Department of Gastric Surgery, Fudan University Shanghai Cancer Center, Shanghai, 200032, China.
Yi DouDepartment of Gastric Surgery, Fudan University Shanghai Cancer Center, Shanghai, 200032, China.
Binhao HuangDepartment of Gastric Surgery, Fudan University Shanghai Cancer Center, Shanghai, 200032, China.
Jing GuoDepartment of Gastric Surgery, Fudan University Shanghai Cancer Center, Shanghai, 200032, China.
Wei KangDepartment of Anatomical and Cellular Pathology, The Chinese University of Hong Kong, Hong Kong, 999077, China.
Caixia ZhuKey Laboratory of Medical Molecular Virology (MOE/NHC/CAMS), School of Basic Medical Sciences, Shanghai Medical College, Biosafety Level 3 Laboratory, Shanghai Institute of Infectious Disease and Biosecurity, Fudan University, Shanghai, 200032, China.
Yuyan WangKey Laboratory of Medical Molecular Virology (MOE/NHC/CAMS), School of Basic Medical Sciences, Shanghai Medical College, Biosafety Level 3 Laboratory, Shanghai Institute of Infectious Disease and Biosecurity, Fudan University, Shanghai, 200032, China.
Donglei ZhouDepartment of Gastric Surgery, Fudan University Shanghai Cancer Center, Shanghai, 200032, China. zhou_dl@sina.com.
Qiliang CaiKey Laboratory of Medical Molecular Virology (MOE/NHC/CAMS), School of Basic Medical Sciences, Shanghai Medical College, Biosafety Level 3 Laboratory, Shanghai Institute of Infectious Disease and Biosecurity, Fudan University, Shanghai, 200032, China. qiliang@fudan.edu.cn.
Dazhi XuDepartment of Gastric Surgery, Fudan University Shanghai Cancer Center, Shanghai, 200032, China. xudzh@fudan.edu.cn.
Fudan University Shanghai Cancer Center · CNShanghai Medical College of Fudan University · CNChinese University of Hong Kong · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundHelicobacter pylori (H pylori) infection is the primary cause of gastric cancer (GC). The role of Disabled-2 (DAB2) in GC remains largely unclear. This study aimed to investigate the role of DAB2 in H pylori-mediated gastric tumorigenesis.

methodsWe screened various datasets of GC to analyze DAB2 expression and cell signaling pathways. DAB2 expression was assessed in human GC tissue microarrays. H pylori infection in vivo and in vitro models were further explored. Immunostaining, immunofluorescence, chromatin immunoprecipitation, co-immunoprecipitation, Western blot, quantitative polymerase chain reaction, and luciferase reporter assays were performed in the current study.

resultsThe bioinformatic analysis verified that DAB2 was 1 of the 8 genes contributed to tumorigenesis and associated with poor prognosis in GC. The median overall survival and disease-free survival rates in DAB2

conclusionsAltogether, these findings indicated that DAB2 is a key mediator in STAT3-regulated translation of YAP1 and plays crucial roles in H pylori-mediated GC development. DAB2 might serve as a novel therapeutic target for GC.

Indexed as

DAB2Gastric cancerH pyloriSTAT3YAP1

Identifiers

PMID38481347
PMCPMC10935867
OpenAlexW4392750881

What OpenQuestion holds

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LicenceCC BY
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Registered trials

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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.