Evidence map›Paper›PMID 40855561›Full record

ArticleJournal of translational medicine2025

Epstein-Barr virus-coded miR-BART19-3p promotes proliferation of EBV-associated gastric cancer by inhibiting GADD45B.

Jing Yang, YueRu Han, Bin Zeng, Guangsheng Hu, Zhifeng Liu, Runliang Gan

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Journal of translational medicine, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
4citing papers in PubMed, 1 pooled it
–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 synthesis or guideline pooled it.

  1. Pooled it
  2. Review
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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

6 authors.

Jing YangDepartment of Gastroenterology, The First Affiliated Hospital of University of South China, Hengyang, 421001, Hunan Province, China.
YueRu HanCancer Research Institute, Hunan Province Key Laboratory of Tumor Cellular and Molecular Pathology, University of South China, Hunan, 421001, China.
Bin ZengDepartment of Gastroenterology, The First Affiliated Hospital of University of South China, Hengyang, 421001, Hunan Province, China.
Guangsheng HuDepartment of Gastroenterology, The First Affiliated Hospital of University of South China, Hengyang, 421001, Hunan Province, China.
Zhifeng LiuDepartment of Otorhinolaryngology, The First Affiliated Hospital of University of South China, Hengyang, 421001, Hunan Province, China. Liuzf@usc.edu.cn.
Runliang GanCancer Research Institute, Hunan Province Key Laboratory of Tumor Cellular and Molecular Pathology, University of South China, Hunan, 421001, China. ganrunliang@usc.edu.cn.ORCID 0009-0007-2587-4379

Funding

Department of Science and Technology of Hunan Province 24A0321Health Commission of Hunan Province B202307019501Hunan Province Cooperative Innovation Center for Molecular Target New Drug Study 2014-405Hunan Provincial Health High-Level Talent Scientific Research Project R2023129Natural Science Foundation of Hunan Province 2021JJ40502Natural Science Foundation of Hunan Province 2023JJ30544Natural Science Foundation of Hunan Province 2025JJ81049and 2025JJ81046
6 · The paper itself

Abstract

backgroundEBV-associated gastric cancer (EBVaGC) is a distinct molecular subtype of gastric cancer with EBV latency infection. EBV microRNAs, especially rightward transcript (BART) microRNAs, play key roles in the tumor growth of EBVaGC. However, the effects of EBV-miR-BART19-3p in EBVaGC remain largely unknown.

methodsEBV-miR-BART19-3p was detected by qRT-PCR in EBER in situ hybridization positive gastric carcinoma tissues. CCK8, Colony formation, EdU and Flow cytometry were conducted in gastric cancer cells with overexpression and knockdown of EBV-miR-BART19-3p compared to the negative control, respectively. Tumor xenografts were conducted in vivo. GADD45B was screened by RNA sequencing and dual-luciferase reporter assays implemented with transfecting EBV-miR-BART19-3p antagomir. Proteins were confirmed by Western blotting.

resultsEBV-miR-BART19-3p was highly expressed in EBVaGC and promoted the proliferation of EBV-associated gastric cancer cells in vitro and accelerated xenograft tumor growth in vivo. Knockdown of EBV-miR-BART19-3p induced cell cycle G2/M phase arrest in AGS EBV cells. Molecularly, EBV-miR-BART19-3p directly targets the 3'-UTR of growth arrest and DNA damage-inducing protein Beta (GADD45B) mRNA and downregulates its protein expression, which consequently reduced cell cycle G2/M phase arrest. Reconstitution of GADD45B can rescue the proliferation phenotype caused by EBV-miR-BART19-3p in EBVaGC cells.

conclusionsOur study indicated Epstein-Barr Virus MicroRNA BART19-3p played an oncogenic role by a novel mechanism of inhibiting GADD45B in EBVaGC, which provides new insights and might be a potential therapeutic strategy for EBVaGC patients.

Indexed as

Antigens, DifferentiationEpstein-Barr Virus InfectionsHerpesvirus 4, HumanMicroRNAsStomach NeoplasmsAnimalsBase SequenceCell Line, TumorCell ProliferationFemaleGADD45 ProteinsGene Expression Regulation, NeoplasticHumansMaleMiceMice, Inbred BALB CAntigens, DifferentiationGADD45B protein, humanGADD45 ProteinsMicroRNAsEBV-associated gastric cancerEpstein-Barr virus-coded miR-BART19-3pGADD45BProliferation

Identifiers

PMID40855561
PMCPMC12376731

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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.