Evidence map›Paper›PMID 39627192›Full record

ArticleNature communications2024

Epstein-Barr virus infection upregulates extracellular OLFM4 to activate YAP signaling during gastric cancer progression.

Fuping Wen, Yi Han, Hui Zhang, Zhangting Zhao, Wenjia Wang, Fan Chen, Weimin Qin, Junyi Ju, Liwei An, Yan Meng and 9 more

Abstract read
In one paragraph

Article in Nature communications, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.

0numbers the graph read from it
0cells of the map it votes in
26citing 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

26 citing papers in PubMed.

  1. Review
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  10. Article
  11. Review
  12. The emerging role of non-Gastroenterology report · 2026
    Review
  13. Review
  14. Article
  15. Review
  16. Review
  17. Review
  18. Review
  19. Article
  20. Olfactomedin 4 in cancer development and progression.Biochimica et biophysica acta. Reviews on cancer · 2025
    Review
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.

Fuping Wen *Department of Stomatology, Shanghai Tenth People's Hospital, Tongji University Cancer Center, Tongji University School of Medicine, Shanghai, 200072, China.ORCID 0009-0005-3153-9820
Yi Han *Department of Stomatology, Shanghai Tenth People's Hospital, Tongji University Cancer Center, Tongji University School of Medicine, Shanghai, 200072, China.
Hui Zhang *State Key Laboratory of Genetic Engineering, School of Life Sciences, Zhongshan Hospital, Fudan University, Shanghai, 200438, China.
Zhangting Zhao *Department of Stomatology, Shanghai Tenth People's Hospital, Tongji University Cancer Center, Tongji University School of Medicine, Shanghai, 200072, China.
Wenjia Wang *State Key Laboratory of Genetic Engineering, School of Life Sciences, Zhongshan Hospital, Fudan University, Shanghai, 200438, China.ORCID 0000-0002-2892-6214
Fan ChenCAS Center for Excellence in Molecular Cell Science, Institute of Biochemistry and Cell Biology, Shanghai Institutes for Biological Sciences, Chinese Academy of Sciences, University of Chinese Academy of Sciences, Shanghai, 200031, China.
Weimin QinState Key Laboratory of Genetic Engineering, School of Life Sciences, Zhongshan Hospital, Fudan University, Shanghai, 200438, China.
Junyi JuDepartment of Stomatology, Shanghai Tenth People's Hospital, Tongji University Cancer Center, Tongji University School of Medicine, Shanghai, 200072, China.
Liwei AnDepartment of Stomatology, Shanghai Tenth People's Hospital, Tongji University Cancer Center, Tongji University School of Medicine, Shanghai, 200072, China.
Yan MengDepartment of Stomatology, Shanghai Tenth People's Hospital, Tongji University Cancer Center, Tongji University School of Medicine, Shanghai, 200072, China.
Jie YangState Key Laboratory of Genetic Engineering, School of Life Sciences, Zhongshan Hospital, Fudan University, Shanghai, 200438, China.
Yang TangDepartment of Stomatology, Shanghai Tenth People's Hospital, Tongji University Cancer Center, Tongji University School of Medicine, Shanghai, 200072, China.
Yun ZhaoCAS Center for Excellence in Molecular Cell Science, Institute of Biochemistry and Cell Biology, Shanghai Institutes for Biological Sciences, Chinese Academy of Sciences, University of Chinese Academy of Sciences, Shanghai, 200031, China.ORCID 0000-0002-7807-6094
Huanhu ZhangDepartment of Digestive Sciences, Shanxi Cancer Hospital, Taiyuan, 030001, China.
Feng LiDepartment of Digestive Sciences, Shanxi Cancer Hospital, Taiyuan, 030001, China.
Wenqi BaiDepartment of Digestive Sciences, Shanxi Cancer Hospital, Taiyuan, 030001, China. wenqibai2022@163.com.ORCID 0000-0002-7142-6805
Yuanzhi XuDepartment of Stomatology, Shanghai Tenth People's Hospital, Tongji University Cancer Center, Tongji University School of Medicine, Shanghai, 200072, China. xuyuanzhi@tongji.edu.cn.ORCID 0009-0000-0572-7100
Zhaocai ZhouState Key Laboratory of Genetic Engineering, School of Life Sciences, Zhongshan Hospital, Fudan University, Shanghai, 200438, China. zhouzhaocai@fudan.edu.cn.ORCID 0000-0002-5441-3922
Shi JiaoState Key Laboratory of Genetic Engineering, School of Life Sciences, Zhongshan Hospital, Fudan University, Shanghai, 200438, China. jiaoshi@fudan.edu.cn.ORCID 0000-0003-3591-8973

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Extracellular vesicles (EVs) are known to mediate cell communications and shape tumor microenvironment. Compared to the well-studied small EVs, the function of large microvesicles (MVs) during tumorigenesis is poorly understood. Here we show the proteome of MVs in Epstein-Barr virus (EBV)-associated gastric cancer (EBVaGC), and identify olfactomedin 4 (OLFM4) is induced by EBV infection and secreted via MVs to promote tumor progression through Hippo signaling. Specifically, OLFM4 is a target gene of the cGAS-STING pathway, and EBV infection activates cGAS-STING pathway and increases OLFM4 expression. Moreover, MV-carried OLFM4 binds with the extracellular cadherin domain of FAT1, thereby impairing its intracellular interaction with MST1 and leading to YAP activation in recipient cells. Together, our study not only reveals a regulatory mechanism though which viral infection is coupled via MVs with intercellular control of the Hippo signaling, but also highlights the OLFM4-Hippo axis as a therapeutic target for EBV-associated cancers.

Indexed as

Adaptor Proteins, Signal TransducingEpstein-Barr Virus InfectionsHerpesvirus 4, HumanSignal TransductionStomach NeoplasmsTranscription FactorsAnimalsCell Cycle ProteinsCell Line, TumorDisease ProgressionExtracellular VesiclesFemaleGene Expression Regulation, NeoplasticGranulocyte Colony-Stimulating FactorHippo Signaling PathwayHumansAdaptor Proteins, Signal TransducingCell Cycle ProteinsGranulocyte Colony-Stimulating FactorOLFM4 protein, humanProtein Serine-Threonine KinasesTranscription FactorsYAP1 protein, humanYAP-Signaling Proteins

Identifiers

PMID39627192
PMCPMC11615309

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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.