ArticleCell death & disease2025
SNRPB promotes gastric cancer progression by regulating aberrant splicing of PUF60.
Article in Cell death & disease, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 2 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
2 citing papers in PubMed.
- Integrated genome-wide high-throughput screening and functional validation identifies Sm proteins as essential splicing regulators for gastric cancer progression.Functional & integrative genomics · 2026Article
- Review
Corrections and comments
- Erratum issued
Authors and funding
15 authors.
Funding
Abstract
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.
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