Silencing of small nuclear ribonucleoprotein polypeptide B inhibits the progression of esophageal squamous cell carcinoma.

Esophageal squamous cell carcinoma (ESCC) is a highly aggressive malignancy with poor prognosis. Small nuclear ribonucleoprotein polypeptide B (SNRPB) has been implicated in the progression of various types of cancer; however, the specific role of this protein in ESCC remains unclear. The present study aimed to investigate the expression and functional significance of SNRPB in ESCC. Bioinformatics analysis was performed to assess SNRPB expression and its clinical relevance in ESCC. Immunohistochemical staining of ESCC tissue samples demonstrated significantly elevated SNRPB expression in tumor tissues, compared with adjacent non-cancerous esophageal tissues. Analysis of public database (TCGA) and institutional clinical data revealed that high SNRPB expression was associated with poor prognosis and advanced clinical stage (T stage), respectively. To evaluate the functional role of SNRPB, a lentivirus-based short hairpin RNA vector was used to inhibit endogenous SNRPB expression in ESCC cell lines. Functional assays, including colony formation, flow cytometry and western blot analysis, demonstrated that SNRPB knockdown significantly inhibited cell proliferation, induced cell cycle arrest and promoted apoptosis. Moreover, molecular analysis indicated that SNRPB knockdown led to modulation of the cell cycle and proteins associated with apoptosis. These findings suggested that SNRPB is a key regulator of ESCC progression, through impacting cell proliferation and apoptosis. Collectively, results of the present study demonstrated that SNRPB may act as a potential prognostic biomarker and therapeutic target for ESCC.