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Pi3k/akt/mtor Signaling in Cancer / HER2/EGFR in Cancer Research / Gastric Cancer Management and Outcomes · Journal article
Peerj · September 11, 2026
Raises a question worth testing. It does not answer one.
This is an in vitro mechanistic study showing that esomeprazole reduces EGF-induced invasion and migration in gastric cancer cell lines, potentially via inhibition of the EGFR/AKT/mTOR pathway. The findings are confined to cultured cells and provide no evidence of clinical efficacy or in vivo effect.
In vitro cell line study. Gastric cancer cell lines. Intervention: Esomeprazole, with or without EGF stimulation; also combined with afatinib. Compared with: EGF-stimulated untreated cells; afatinib alone; combination therapy versus monotherapy.
ESO significantly reduced migration and invasion in GC cells induced by EGF ESO reduced expression levels of N-cadherin, MMP2, MMP9, Vimentin, p-EGFR, p-AKT, and p-mTOR Combination of ESO and afatinib produced more pronounced reduction in cell viability, invasion, migration, and protein expression than either treatment alone
Safety was not reported in the material analysed. Check the source before drawing any conclusion about harm.
The source did not state who this applies to in practice.
In vitro mechanistic study demonstrating that esomeprazole modulates a signaling pathway implicated in gastric cancer cell invasion; raises a question about therapeutic potential rather than answering one in a clinical or animal model.
As stated by the source record.
Graded across the dimensions that decide whether you should act, each from what the source actually supports. There is no single score, and where a dimension was not assessed it says so.
What is missing. This record has no reported figures. That is a gap in the analysis, not a judgement about the study.
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 via the EGFR/AKT/mTOR pathway, offering a potential new strategy for GC treatment.
Taken from the source record, never inferred. Follow any of these and new work involving them reaches your briefing.