ArticleiScience2025
Alternative splicing of EZH2 regulated by SNRPB mediates hepatocellular carcinoma progression via BMP2 signaling pathway.
Article in iScience, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 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
- HnRNP A1 and A2B1 enforce Ezh2 mRNA splicing to promote germinal center B cell responses.Nature communications · 2026Article
- Comprehensive Evaluation and Validation Reveal Mitochondrial Solute Carrier SLC25A3 as a Novel Prognostic Biomarker and Therapeutic Target in Hepatocellular Carcinoma.Journal of hepatocellular carcinoma · 2026Article
- Genome-wide CRISPR screen identifies splicing factor SF3B4 in driving hepatocellular carcinoma.Science advances · 2025Article
- Nanopore Sequencing Reveals Novel Alternative Splice Variants of EZH2 in Pediatric Medulloblastoma.Biomedicines · 2025Article
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Authors and funding
11 authors.
Funding
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Abstract
Increasing evidence suggests that aberrant alternative splicing plays crucial roles in tumorigenesis. However, the function of EZH2 splice variants as well as the mechanism by which EZH2 alternative splicing occurs in hepatocellular carcinoma (HCC) remain elusive. Here, we analyzed both our own and published transcriptomic data, obtaining 19 splice variants of EZH2 in addition to canonical full-length EZH2-A in HCC. We found that expression of EZH2-A/EZH2-B in tumor tissues and cell lines was significantly higher than in normal tissues. Conversely, EZH2-C expression was lower in tumor tissues and cell lines than in normal tissues. Further functional analysis indicated that unlike full-length EZH2-A that promotes H3K27 methylation, EZH2-C reduced H3K27me3 levels. EZH2-C inhibited proliferation, migration, invasion of HCC cells. Moreover, EZH2-A and EZH2-C regulate the BMP2 signaling pathway oppositely. Mechanistically, EZH2's alternative splicing was mediated by splicing factor SNRPB. In summary, this study revealed that alternative splicing of EZH2 regulates HCC.
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