Evidence map›Paper›PMID 41528639›Full record

ArticleCellular oncology (Dordrecht, Netherlands)2026

IRF1 suppresses gastric tumorigenesis via dual PI3K/AKT-ERK pathway modulation and functional antagonism of oncogenic MX2.

Wenjing Chen, Neng Lou, Xietao Chen, Xianjing Hu, Chenchen Mao, Jiaqi Yang, Jun Cheng, Chenbin Chen, Xiangyang Xue, Xian Shen

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Cellular oncology (Dordrecht, Netherlands), 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing 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

1 citing paper in PubMed.

  1. Article
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

10 authors.

Wenjing Chen *Department of Gastrointestinal Surgery, First Affiliated Hospital, Wenzhou Medical University, Wenzhou, China.
Neng Lou *Department of Microbiology and Immunology, Institute of Molecular Virology and Immunology, Institute of Tropical Medicine, Wenzhou Medical University, Wenzhou, China.
Xietao Chen *Department of Gastrointestinal Surgery, First Affiliated Hospital, Wenzhou Medical University, Wenzhou, China.
Xianjing HuDepartment of Anesthesiology and Perioperative Medicine, The Second Affiliated Hospital, Yuying Children's Hospital of Wenzhou Medical University, Wenzhou, Zhejiang, China.
Chenchen MaoDepartment of Microbiology and Immunology, Institute of Molecular Virology and Immunology, Institute of Tropical Medicine, Wenzhou Medical University, Wenzhou, China.
Jiaqi YangDepartment of Microbiology and Immunology, Institute of Molecular Virology and Immunology, Institute of Tropical Medicine, Wenzhou Medical University, Wenzhou, China.
Jun ChengDepartment of Gastrointestinal Surgery, First Affiliated Hospital, Wenzhou Medical University, Wenzhou, China.
Chenbin ChenDepartment of Gastrointestinal Surgery, First Affiliated Hospital, Wenzhou Medical University, Wenzhou, China.
Xiangyang XueDepartment of Microbiology and Immunology, Institute of Molecular Virology and Immunology, Institute of Tropical Medicine, Wenzhou Medical University, Wenzhou, China. wzxxy@wmu.edu.cn.
Xian ShenDepartment of Gastrointestinal Surgery, First Affiliated Hospital, Wenzhou Medical University, Wenzhou, China. 13968888872@163.com.

Funding

Key Research and Development Program of Zhejiang Province 2021C03120National Natural Science Foundation of China 32470969Wenzhou Municipal Science and Technology Bureau Y20220860, Y20220894
6 · The paper itself

Abstract

backgroundInterferon regulatory factor 1 (IRF1) plays a crucial role in the type I interferon (IFN) response. However, its functional role and underlying mechanisms in gastric cancer (GC) remain unclear. This study aims to investigate the biological significance of IRF1 in GC progression and its potential as a therapeutic target.

methodsIRF1 expression was analyzed using The Cancer Genome Atlas (TCGA) and GTEx databases, validated by immunohistochemistry (IHC) in 366 GC patients. Functional experiments, including CCK-8, Transwell migration and invasion assays, and apoptosis analysis, were conducted in GC cell lines with IRF1 overexpression or knockdown. A subcutaneous xenograft model was established to evaluate the in vivo effects of IRF1 on tumor growth. Co-immunoprecipitation and western blotting were performed to explore the molecular interactions between IRF1 and Myxovirus resistance 2 (MX2), as well as its regulation of the PI3K signaling pathway.

resultsIRF1 expression was significantly higher in gastric cancer tissues than in adjacent normal tissues. Higher IRF1 levels were also associated with improved patient survival. Overexpression of IRF1 inhibited GC cell proliferation, migration, and invasion while promoting apoptosis, whereas IRF1 knockdown had the opposite effects. Mechanistically, IRF1 suppressed PI3K/p-AKT signaling while enhancing p-ERK1/2 activation. Moreover, IRF1 directly interacted with MX2, a protein involved in epithelial-mesenchymal transition (EMT), and this interaction was essential for suppressing MX2-mediated oncogenic activity. In vivo experiments confirmed that IRF1 overexpression significantly reduced tumor growth and metastasis.

conclusionsIRF1 functions as a tumor suppressor in GC by modulating the PI3K signaling pathway and interacting with MX2 to inhibit EMT. These findings highlight IRF1 as a potential therapeutic target for GC treatment.

Indexed as

CarcinogenesisInterferon Regulatory Factor-1MAP Kinase Signaling SystemMyxovirus Resistance ProteinsPhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktStomach NeoplasmsAnimalsApoptosisCell Line, TumorCell MovementCell ProliferationEpithelial-Mesenchymal TransitionFemaleGene Expression Regulation, NeoplasticHumansInterferon Regulatory Factor-1IRF1 protein, humanMyxovirus Resistance ProteinsPhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktEMTGastric cancerIRF1MX2PI3K signalingTumor suppressionType i interferon response

Identifiers

PMID41528639
PMCPMC12799679

What OpenQuestion holds

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LicenceCC BY-NC-ND
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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.