SEC31A promotes gastric cancer progression by inducing the PI3K/AKT/mTOR pathway and enhancing the CCL5‑mediated M2 polarization and recruitment of tumor‑associated macrophages

SEC31A is overexpressed in gastric cancer tissue and cell lines, and its knockdown reduces epithelial-mesenchymal transition, proliferation, migration and invasion of GC cells. SEC31A activates the PI3K/AKT/mTOR pathway, since the PI3K inhibitor LY294002 counteracts its effects, and it drives CCL5-mediated M2 polarization and recruitment of tumor-associated macrophages in co-cultures of THP-1 and GC cells. Reduced SEC31A expression improved the efficacy of anti-PD-1 therapy in GC models, positioning SEC31A as a potential prognostic marker and immunotherapy target.