SRSF10 promotes cisplatin resistance in bladder cancer via BIN1 Exon 12 retention and ANXA1 activation - PubMed
6 hours ago
- #Cisplatin Resistance
- #Alternative Splicing
- #Bladder Cancer
- SRSF10 is overexpressed in bladder cancer and linked to poor prognosis and advanced clinical stages.
- Knockdown of SRSF10 reduces cell proliferation and cisplatin resistance (lower IC50), while overexpression increases these effects, validated in models and clinical samples.
- Mechanistically, SRSF10 causes retention of BIN1 exon 12, upregulating the BIN1(12+) isoform, which interacts with and activates ANXA1 to promote cisplatin resistance.
- The study identifies the SRSF10/BIN1(12+)/ANXA1 signaling axis as a key driver of cisplatin resistance in bladder cancer, suggesting SRSF10 as a potential therapeutic target.