ArticleOncogene2023
The splicing factor SNRPB promotes ovarian cancer progression through regulating aberrant exon skipping of POLA1 and BRCA2.
Article in Oncogene, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
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Who cites it
22 citing papers in PubMed, 21 citations in OpenAlex.
- Deconvoluting the multi-faceted roles of alternative splicing events in cancer: From underlying mechanisms to innovative therapeutics.Acta pharmaceutica Sinica. B · 2026Review
- Integrated genome-wide high-throughput screening and functional validation identifies Sm proteins as essential splicing regulators for gastric cancer progression.Functional & integrative genomics · 2026Article
- Disruption of the SNRPF-DDX24-E2F4 Feedback Loop Uncouples Splicing and Transcriptional Regulation to Suppress Ovarian Cancer Progression.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- SNRPD2-CPSF7-UBE2K axis drives ovarian cancer progression via alternative splicing-polyadenylation crosstalk.Oncogene · 2026Article
- Spliceosomal component SNRPE drives cell proliferation by regulating CTP synthase 1 mRNA splicing in ovarian cancer.Oncogene · 2026Article
- Silencing of small nuclear ribonucleoprotein polypeptide B inhibits the progression of esophageal squamous cell carcinoma.Oncology letters · 2026Article
- Indel pattern-guided repair mapping reveals genome-wide DNA repair networks in CRISPR/Cas9 editing.Nucleic acids research · 2026Article
- SNRPD2-mediated regulation of DDX39B splicing promotes endometrial cancer progression by suppressing the activation of CTSC cryptic exons.Cell death & disease · 2026Article
- Nonsense-mediated mRNA decay: a key regulatory system engaged in cancer.Cell communication and signaling : CCS · 2025Review
- Spliceosomal GTPase EFTUD2 mediates DDX41 intron retention to promote the malignant progression of ovarian cancer.British journal of cancer · 2025Article
- SNRPB/CCNB1 axis promotes hepatocellular carcinoma progression and cisplatin resistance through enhancing lipid metabolism reprogramming.Journal of experimental & clinical cancer research : CR · 2025Article
- Review
- SNRPB-mediated regulation of DDX39A splicing promotes ovarian cancer progression by regulating α6 integrin subunit expression.Oncogene · 2025Article
- Targeting the splicing factor SNRPB inhibits endometrial cancer progression by retaining the POLD1 intron.Experimental & molecular medicine · 2025Article
- Single-cell dual-omics reveals translational and transcriptional landscapes and regulations in oocytes from ovarian endometriosis patients.Frontiers in endocrinology · 2025Article
- CPSF4-mediated regulation of alternative splicing of HMG20B facilitates the progression of triple-negative breast cancer.Journal of translational medicine · 2024Article
- Article
- Identifying the prognostic significance of mitophagy-associated genes in multiple myeloma: a novel risk model construction.Clinical and experimental medicine · 2024Article
- Alternative splicing in ovarian cancer.Cell communication and signaling : CCS · 2024Review
- Deciphering the role of sphingolipid metabolism in the immune microenvironment and prognosis of esophageal cancer via single-cell sequencing and bulk data analysis.Discover oncology · 2024Article
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Authors and funding
8 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Splicing factors play a crucial role in the initiation and development of various human cancers. SNRPB, a core spliceosome component, regulates pre-mRNA alternative splicing. However, its function and underlying mechanism in ovarian cancer remain unclear. This study identified SNRPB as a critical driver of ovarian cancer through TCGA and CPTAC database analysis. SNRPB was highly upregulated in fresh frozen ovarian cancer tissues compared with normal fallopian tubes. Immunohistochemistry revealed that SNRPB expression was increased in formalin-fixed, paraffin-embedded ovarian cancer sections and was positively correlated with a poor prognosis for ovarian cancer. Functionally, SNRPB knockdown suppressed ovarian cancer cell proliferation and invasion, and overexpression exerted opposite effects. SNRPB expression increased after cisplatin treatment, and silencing SNRPB sensitized ovarian cancer cells to cisplatin. KEGG pathway analysis revealed that the differentially expressed genes (DEGs) were mainly enriched in DNA replication and homologous recombination, and almost all DEGs related to DNA replication and homologous recombination were downregulated after SNRPB knockdown according to RNA-seq. Exon 3 skipping of the DEGs DNA polymerase alpha 1 (POLA1) and BRCA2 was induced by SNRPB silencing. Exon 3 skipping of POLA1 yielded premature termination codons and led to nonsense-mediated RNA decay (NMD); exon 3 skipping of BRCA2 led to loss of the PALB2 binding domain, which is necessary for homologous recombination, and increased ovarian cancer cell cisplatin sensitivity. POLA1 or BRCA2 knockdown partially impaired the increased malignancy of SNRPB-overexpressing ovarian cancer cells. Moreover, miR-654-5p was found to reduce SNRPB mRNA expression by directly binding to the SNRPB 3'-UTR. Overall, SNRPB was identified as an important oncogenic driver that promotes ovarian cancer progression by repressing exon 3 skipping of POLA1 and BRCA2. Thus, SNRPB is a potential treatment target and prognostic marker for ovarian cancer.
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