ArticleMolecular and cellular biochemistry2025
YTHDC1 orchestrates oncogenic splicing via the CLK1-SRSF1 splicing machinery to regulate castration-resistant prostate cancer progression.
Article in Molecular and cellular biochemistry, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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Who cites it
3 citing papers in PubMed.
- Targeting the Androgen Receptor and Associated Cofactors in Prostate Cancer: Novel Approaches and Future Perspectives.International journal of molecular sciences · 2026Review
- Integrative analysis of YTHDC1 phosphoproteome unveils its phosphomodulatory network linked to splicing and tumorigenesis.Frontiers in bioinformatics · 2026Article
- Integrative analysis identifies FBXO5 as a critical mediator of CRPC progression and bone metastatic potential.Discover oncology · 2025Article
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Authors and funding
10 authors.
Funding
Abstract
Androgen receptor variant 7 (AR-V7) plays a critical role in castration-resistant prostate cancer (CRPC) progression even under androgen-deprivation conditions. Clinical and experimental studies have established that AR-V7 expression is a critical driver of CRPC progression and resistance to first-line anti-androgen therapy including enzalutamide. Understanding the mechanisms regulating AR-V7 generation and its contribution to drug resistance is critical for developing newer approaches to target CRPC. In this study, we have investigated the role of the RNA-binding protein YTHDC1, a m6A reader, in regulating AR-V7 splicing. Our findings reveal that YTHDC1 is overexpressed in CRPC and modulating its expression directly affects AR-V7 levels, rendering the cells sensitive to enzalutamide treatment. Mechanistically, we demonstrate that YTHDC1 binds to the AR-V7 pre-mRNA and facilitates the recruitment of phosphorylated SRSF1, a splice factor that promotes AR-V7 splicing. Additionally, we also demonstrate that it modulates the levels of CLK1, a known SRSF1 kinase supporting its role in regulating AR-V7 splicing. Furthermore, our experiments also reveal that YTHDC1 regulates the expression of other oncogenic transcripts, including Bcl-2, Cyclin D1, Nova1, and VEGF-A, highlighting its broader role in cancer progression. Overall, our study supports that targeting YTHDC1 could be a novel therapeutic approach to overcome AR-V7-mediated treatment resistance in CRPC patients.
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Registered trials
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