Evidence map›Paper›PMID 41317224›Full record

ArticleDigestive diseases and sciences2026

Helicobacter pylori Lipopolysaccharide Upregulates MDM2 via the TLR4/MAPK/AP-1 Pathway to Promote Gastric Cancer Progression.

Yuqin Li, Lin Xu, Xiaolan Lu, Baiqing Fu, Qiuyu Jiang, Wujun Xiong, Wenqing Tang, Dejun Wu

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Article in Digestive diseases and sciences, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing 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

4 citing papers in PubMed.

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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

8 authors.

Yuqin Li *Department of Gastroenterology, Shanghai Pudong Hospital, Fudan University Pudong Medical Center, Shanghai, China.
Lin Xu *Department of Gastroenterology and Hepatology, Zhongshan Hospital, Fudan University, Shanghai, China.
Xiaolan LuDepartment of Gastroenterology, Shanghai Pudong Hospital, Fudan University Pudong Medical Center, Shanghai, China.
Baiqing FuDepartment of Gastroenterology, Shanghai Pudong Hospital, Fudan University Pudong Medical Center, Shanghai, China.
Qiuyu JiangDepartment of Gastroenterology and Hepatology, Zhongshan Hospital, Fudan University, Shanghai, China.
Wujun XiongDepartment of Gastroenterology, Shanghai Pudong Hospital, Fudan University Pudong Medical Center, Shanghai, China.
Wenqing TangDepartment of Gastroenterology and Hepatology, Zhongshan Hospital, Fudan University, Shanghai, China. tang.wenqing@zs-hospital.sh.cn.
Dejun WuDepartment of Gastrointestinal Surgery, Shanghai Pudong Hospital, Fudan University Pudong Medical Center, Shanghai, China. wudejun20565@163.com.

Funding

the Discipline Construction Promoting Project of Shanghai Pudong Hospital Tszb2023-01the Discipline Construction Promoting Project of Shanghai Pudong Hospital Zdzk2020-10the Medical Discipline Construction Program of Shanghai Pudong New Area Health Commission(the Public Health Disciplines Program) PWGw2025-01the Science and Technology Development Fund of Shanghai Pudong New Area PKJ2021-Y38
6 · The paper itself

Abstract

backgroundThe lipopolysaccharide (LPS) of Helicobacter pylori (HP) is a critical virulence factor in gastric cancer development. As a toxic component of the HP cytoderm, HP LPS causes persistent inflammatory injury to the gastric mucosa. Although HP lipopolysaccharide exhibits weaker endotoxic activity, it still promotes gastric cancer progression by inducing chronic inflammation and enhancing cellular proliferation. However, the specific signaling pathways involved are not fully understood.

methodsGES-1, HGC-27, and MKN-45 cells were treated with LPS from HP and E. coli. Western blotting and a luciferase reporter assay were used to analyze MDM2 expression and transcriptional activity. Cell proliferation, migration, and invasion were evaluated through colony formation, scratch wound healing, and transwell assays. Immunohistochemistry was used to examine MDM2 and p53 expression, while immunofluorescence detected regulatory T cells. Gastric cancer mouse models were also used to confirm MDM2's role in gastric cancer.

resultsHP infection resulted in elevated MDM2 levels in gastric precancerous lesions and cancers. HP LPS enhances MDM2 expression in GC cells. This effect is mediated through TLR4/MAPK/AP-1, which promotes the proliferation and invasion of gastric cancer cells. In addition, MDM2 participated in Tregs infiltration and promoted the maintenance of an immunosuppressive tumor microenvironment in gastric cancer.

conclusionsHP LPS enhances MDM2 expression in GC cells through the TLR4/MAPK/AP-1 pathway. MDM2 mediates the protumor effects of HP LPS by promoting tumor cell proliferation and regulating Treg-mediated immune suppression. Our study deepens the understanding of gastric cancer progression and identifies MDM2 as an effective therapeutic target.

Indexed as

Helicobacter InfectionsHelicobacter pyloriLipopolysaccharidesProto-Oncogene Proteins c-mdm2Stomach NeoplasmsToll-Like Receptor 4Transcription Factor AP-1AnimalsCell Line, TumorCell ProliferationDisease ProgressionHumansMiceSignal TransductionUp-Regulationlipopolysaccharide, Helicobacter pyloriLipopolysaccharidesMDM2 protein, humanProto-Oncogene Proteins c-mdm2TLR4 protein, humanToll-Like Receptor 4Transcription Factor AP-1Gastric cancerLipopolysaccharideMDM2Tumorigenesis

Identifiers

PMID41317224

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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.