SNRPB promotes gastric cancer progression via the ECM receptor signaling pathway

Gastric Cancer (GC) ranks among the most common and deadly malignancies globally. Small nuclear ribonucleoprotein polypeptide (SNRPB), a core spliceosomal component, was recently identified as essential for GC cell survival, although its mechanisms remain unclear. This study investigated the functions of SNRPB in GC progression and explored its underlying molecular mechanisms. SNRPB expression in GC tissues and adjacent non-cancerous tissues from 48 patients was analyzed via immunohistochemistry. SNRPB was significantly overexpressed in GC tissues compared with its expression in adjacent normal tissues, and higher SNRPB expression was associated with tumor stage and metastasis. Survival data obtained from the Kaplan-Meier Plotter website demonstrated that patients with GC and high SNRPB expression had a worse prognosis. Patient-derived organoids (PDOs) were successfully established from three patients with GC. These PDO models faithfully recapitulated the histological and genetic features of the original tumors. Notably, SNRPB knockdown in organoids significantly impaired Organoid formation, demonstrating its essential role in maintaining tumor growth capacity. Complementary experiments in conventional 2D cultures illustrated that SNRPB knockdown reduced cell proliferation and migration. Mechanistically, transcriptomic analysis revealed that SNRPB silencing downregulated multiple genes involved in the extracellular matrix (ECM) receptor signaling pathway, thereby impairing tumor progression. In conclusion, our study identifies SNRPB as a key regulator of GC development through the ECM receptor signaling pathway, suggesting its potential as a therapeutic target.

Extracellular matrix receptor signaling; Gastric cancer; Patient-derived organoid; SNRPB; Tumor progression.