Evidence map›Paper›PMID 41691064›Full record

ArticleScientific reports2026

Chronic inflammation promotes gastric cancer progression via ADAM10-mediated cleavage of CX3CL1.

Zhiyuan Song, Yueying Liu, Zan Wang, Sicheng Zhao, Jingcheng Zhang, Yunhai Wei, Zhengqi Zhao, Tao Jiang, Guangji Zhang

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Scientific reports, 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

9 authors.

Zhiyuan Song *School of Basic Medical Sciences, Zhejiang Chinese Medical University, Hangzhou, 310053, China.
Yueying Liu *School of Basic Medical Sciences, Zhejiang Chinese Medical University, Hangzhou, 310053, China.
Zan Wang *School of Basic Medical Sciences, Zhejiang Chinese Medical University, Hangzhou, 310053, China.
Sicheng ZhaoSchool of Basic Medical Sciences, Zhejiang Chinese Medical University, Hangzhou, 310053, China.
Jingcheng ZhangSchool of Basic Medical Sciences, Zhejiang Chinese Medical University, Hangzhou, 310053, China.
Yunhai WeiHuzhou Central Hospital, Affliated Central Hospital Huzhou University, Huzhou, 313000, China.
Zhengqi ZhaoSchool of Basic Medical Sciences, Zhejiang Chinese Medical University, Hangzhou, 310053, China.
Tao JiangSchool of Basic Medical Sciences, Zhejiang Chinese Medical University, Hangzhou, 310053, China. jt_tcm@163.com.
Guangji ZhangSchool of Basic Medical Sciences, Zhejiang Chinese Medical University, Hangzhou, 310053, China. zgjtcm@zcmu.edu.cn.

Funding

Key project of the National Nature Foundation of China 82030119Key Support Project of Regional Innovation and Development Joint Fund of National Natural Science Foundation of China U23A20499National Natural Science Foundation of China 82204950State Administration of Traditional Chinese Medicine Science and Technology Department - Zhejiang Provincial Administration of Traditional Chinese Medicine joint science and technology plan key research project GZY-ZJ-KJ-23094Zhejiang Chinese Medicine University Chunyan Special Fund for the development of traditional Chinese medicine CY202302Zhejiang Provincial Natural Science Foundation of China LQ23H270013
6 · The paper itself

Abstract

This study aimed to investigate the impact of chronic inflammation (CI) on gastric cancer (GC) progression and the underlying molecular mechanisms. A subcutaneous xenograft model using 615-strain mice was established to evaluate the pro-tumorigenic effects of CI. Proteome Profiler Mouse XL Cytokine Array was used to screen for key pro-tumorigenic cytokines induced by CI, and ELISA was employed for validation. single-cell RNA sequencing(ScRNA-seq) was performed to identify the cellular source of CX3CL1 in GC tumor tissues. CCK-8 and colony formation assays were used to assess the effect of CX3CL1 on GC cell proliferation, while wound-healing and Transwell assays evaluated cell migration. ADAM10 expression was measured in gastric cancer cells and tissues via qRT-PCR, Western blot, and immunofluorescence staining. CI significantly accelerated gastric cancer progression. CX3CL1 expression was markedly higher in GC tissues than in normal gastric tissues, and high CX3CL1 expression was associated with poor prognosis in GC patients. CX3CL1 recombinant protein significantly promoted the proliferation and migration of GC cells, and these effects were attenuated by pharmacological inhibition of CX3CR1. Mechanistically, CI upregulated the expression of ADAM10, which plays a key role in converting membrane-bound CX3CL1 to its soluble form. This study provided evidence that chronic inflammation could promote tumor progression through the activation of ADAM10/CX3CL1 axis in gastric cancer.

Indexed as

ADAM10 ProteinAmyloid Precursor Protein SecretasesChemokine CX3CL1InflammationMembrane ProteinsStomach NeoplasmsAnimalsCell Line, TumorCell MovementCell ProliferationChronic DiseaseDisease ProgressionFemaleGene Expression Regulation, NeoplasticHumansMaleADAM10 ProteinADAM10 protein, humanAmyloid Precursor Protein SecretasesChemokine CX3CL1CX3CL1 protein, humanMembrane ProteinsADAM10Chronic inflammationCX3CL1Gastric cancer

Identifiers

PMID41691064
PMCPMC12996507

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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.