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

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.