ArticleFrontiers in oncology2025
HPV-driven transcriptome and splicing rewiring under SRPK1 inhibition in cervical cancer.
Article in Frontiers in oncology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Background: Serine/arginine protein kinase 1 phosphorylates serine-arginine-rich (SR) proteins to regulate splice-site selection during alternative splicing. While its role in general RNA regulation is established, its contribution to the HPV-dependent transcriptome and splicing stratification in cervical cancer remains unclear. Therefore, we sought to determine how SRPK1 inhibition differentially remodels gene expression and alternative splicing in HPV Methods: HPV16 Results: SRPK1 inhibition was associated with distinct responses that were HPV-related. In C33A cells, upregulated genes were enriched for translation, RNA processing, and glycosylation, with KEGG highlighting ribosome and metabolic modules. Ribosomal hubs dominated the PPI/MCODE, suggesting possible translational and metabolic adjustments. In contrast, SiHa cells exhibited transcriptomic changes consistent with reduced expression of genes linked to Hippo, Wnt, PI3K-AKT, ERK1/2 signaling, migration, angiogenesis, and growth factor cytokine networks. Targets of YAP/TAZ (e.g., Conclusion: SRPK1 inhibition may remodel the cervical cancer transcriptome in an HPV-linked manner, with SiHa cells exhibiting changes consistent with suppression of oncogenic signaling, whereas C33A cells adapt through translational and metabolic reprogramming.
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