ArticleJournal of advanced research2026
SRSF9 mediates oncogenic RNA splicing of SLC37A4 via liquid-liquid phase separation to promote oral cancer progression.
Article in Journal of advanced research, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed.
- The CDKL5 kinase undergoes liquid-liquid phase separation driven by a serine-rich C-terminal region.Life science alliance · 2026Article
- hnRNPA1-SF3B3 interaction drives radioresistance in oral squamous cell carcinoma by modulating MARF1 alternative splicing isoforms.Journal of experimental & clinical cancer research : CR · 2026Article
- Exploring Disordered Regions of Human Spliceosome Proteins.The journal of physical chemistry letters · 2026Article
- Alternative Splicing: Molecular Mechanisms, Biological Functions, Diseases, and Potential Therapeutic Targets.MedComm · 2025Review
- Article
- Biomolecular phase separation in tumorigenesis: from aberrant condensates to therapeutic vulnerabilities.Molecular cancer · 2025Review
- Article
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20 authors.
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Abstract
introductionOral cancer represents a significant proportion of head and neck malignancies, accounting for approximately 3 % of all malignant tumors worldwide.
objectivesAlternative splicing (AS), a post-transcriptional regulatory mechanism, is increasingly linked to cancer development. The precise impact of AS on oral cancer progression is not well understood.
methodsBioinformatics, semi-quantitative RT-PCR, and minigene reporter system to detect the skipping of SLC37A4 exon 7 in oral cancer. FRAP, live cell immunofluorescence demonstrates that SRSF9 can undergo liquid-liquid phase separation (LLPS). In vivo and in vitro experiments with subcutaneous graft tumors, CCK8, EdU, transwell, and others were used to detect the effects of SRSF9 and its induced SLC37A4-S isoforms on the malignant phenotype of oral cancer cells.
resultsOur investigation revealed a multitude of aberrant alternative splicing events within head and neck tumor tissues, most notably the pronounced skipping of exon 7 in the SLC37A4 gene. This splicing anomaly leads to the production of a truncated isoform, SLC37A4-S, which is associated with a poor prognosis and significantly augments the proliferation and metastatic potential of oral cancer cells relative to the wild-type isoform, SLC37A4-L. Mechanically, SRSF9 may play a regulatory role in the aberrant splicing of SLC37A4. Furthermore, SRSF9 is capable of undergoing LLPS, a process driven by its arginine-serine-rich (RS) domain. Disruption of SRSF9 LLPS through the use of inhibitors or mutants effectively prevents its regulatory influence on the splicing of SLC37A4. Significantly, our research demonstrates that both SRSF9 and its regulated splicing isoforms of SLC37A4-S contribute to cisplatin chemotherapy resistance in oral cancer cells.
conclusionThis study elucidates the mechanism by which SRSF9 phase separation mediates splicing in oral cancer, thereby establishing a basis for considering SRSF9 and its associated SLC37A4-S isoforms as potential therapeutic targets for oral cancer treatment.
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