Evidence map›Paper›PMID 42741692›Full record

ArticlePeerJ2026

Esomeprazole inhibits EGF-induced invasion and migration of gastric cancer cells.

Fangfang Huang, Jinfeng Du, Xuanruo Zhang, Mengru Tian, Qiangqiang Lv, Xiufeng Chu, Hongqiao Zhang, Zisen Zhang

Abstract read
In one paragraph

Article in PeerJ, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
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0citing papers in PubMed
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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

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3 · Its place in the literature

Who cites it

0 citing papers in PubMed.

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4 · The record

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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.

Fangfang HuangZhengzhou Key Laboratory of Lipid Metabolism and Precision Diagnosis & Treatment in Oncology, Oncology Department, the Fifth Affiliated Hospital of Zhengzhou University, Zhengzhou, Henan, China.
Jinfeng DuChongqing Emergency Medical Center, Chongqing, China.
Xuanruo ZhangZhengzhou Key Laboratory of Lipid Metabolism and Precision Diagnosis & Treatment in Oncology, Oncology Department, the Fifth Affiliated Hospital of Zhengzhou University, Zhengzhou, Henan, China.
Mengru TianZhengzhou Key Laboratory of Lipid Metabolism and Precision Diagnosis & Treatment in Oncology, Oncology Department, the Fifth Affiliated Hospital of Zhengzhou University, Zhengzhou, Henan, China.
Qiangqiang LvZhengzhou Key Laboratory of Lipid Metabolism and Precision Diagnosis & Treatment in Oncology, Oncology Department, the Fifth Affiliated Hospital of Zhengzhou University, Zhengzhou, Henan, China.
Xiufeng ChuZhengzhou Key Laboratory of Lipid Metabolism and Precision Diagnosis & Treatment in Oncology, Oncology Department, the Fifth Affiliated Hospital of Zhengzhou University, Zhengzhou, Henan, China.
Hongqiao ZhangZhengzhou Key Laboratory of Lipid Metabolism and Precision Diagnosis & Treatment in Oncology, Oncology Department, the Fifth Affiliated Hospital of Zhengzhou University, Zhengzhou, Henan, China.
Zisen ZhangZhengzhou Key Laboratory of Lipid Metabolism and Precision Diagnosis & Treatment in Oncology, Oncology Department, the Fifth Affiliated Hospital of Zhengzhou University, Zhengzhou, Henan, China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Background: Gastric cancer (GC) is one of the most prevalent and lethal malignancies worldwide, with invasion and metastasis being the key factors contributing to its poor prognosis and high mortality rates. Epidermal growth factor (EGF)-induced activation of EGFR and downstream AKT/mTOR signaling plays a central role in promoting cancer cell invasion and migration. While epidermal growth factor receptor (EGFR)-targeted therapies such as afatinib effectively inhibit these processes, the potential of esomeprazole (ESO) to modulate GC metastasis has not been fully elucidated. This study aims to investigate the inhibitory effect of ESO on EGF-induced invasion and migration of gastric cancer cells, and its relationship with the EGFR/protein kinase B (AKT)/mechanistic target of rapamycin (mTOR) signaling pathway. Methods: Cell viability, invasion, migration and protein expression were assessed using cell counting kit-8 (CCK-8) assay, Transwell assay, wound healing assay and western blot. Results: ESO significantly reduced migration and invasion in GC cells, as well as the expression levels of N-cadherin, MMP2, MMP9, Vimentin, p-EGFR, p-AKT, and p-mTOR induced by EGF. The combination of ESO and afatinib (an irreversible EGFR inhibitor) led to a more pronounced reduction in cell viability, invasion, migration, and protein expression compared to either treatment alone. Conclusions: ESO inhibits EGF-induced invasion and migration in GC cells potentially

Indexed as

Cell MovementEpidermal Growth FactorEsomeprazoleStomach NeoplasmsCadherinsCell Line, TumorCell SurvivalErbB ReceptorsHumansMatrix Metalloproteinase 2Matrix Metalloproteinase 9Neoplasm InvasivenessProto-Oncogene Proteins c-aktSignal TransductionTOR Serine-Threonine KinasesVimentinCadherinsEGFR protein, humanEpidermal Growth FactorErbB ReceptorsEsomeprazoleMatrix Metalloproteinase 2Matrix Metalloproteinase 9MTOR protein, humanProto-Oncogene Proteins c-aktTOR Serine-Threonine KinasesVimentinAfatinibEGFR/AKT/mTOREpidermal growth factorEsomeprazoleGastric cancerInvasionMigration

Identifiers

PMID42741692
PMCPMC13573768

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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.