SNRPB promotes gastric cancer progression by regulating aberrant splicing of PUF60.

Alternative splicing is a pivotal regulatory mechanism in cellular biology that critically influences the tumorigenesis, progression, and phenotypic diversity of cancer. This study aimed to assess the intricate details and regulatory mechanisms of alternative splicing in gastric cancer. We constructed a comprehensive map of aberrant alternative splicing events in gastric cancer through bioinformatic analysis of public databases and clinical samples. Our study identified many abnormal splicing events in gastric cancer tissues, with exon skipping being the most frequent event. SNRPB, a key spliceosome component and principal splicing factor, was associated with the aberrant splicing of numerous splicing factors and oncogenes, influencing the p53 signaling pathway in the development and progression of gastric cancer. SNRPB directly regulates the selective splicing of TP53 by modulating its downstream factor, PUF60, thus facilitating the initiation and progression of gastric cancer. Therefore, SNRPB overexpression is linked to poor prognosis in gastric cancer and is a potential biomarker and therapeutic target.