ArticlePeerJ2026
Esomeprazole inhibits EGF-induced invasion and migration of gastric cancer cells.
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.
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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.
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Authors and funding
8 authors.
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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
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