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TUT1 promotes PDAC progression through Alternative Splicing [3‘-seq]

GSE212513 Mus musculus Expression profiling by high throughput sequencing 4 samples Submitted 2025/01/11 Platform GPL21273
Summary
Pancreatic ductal adenocarcinoma (PDAC) is a malignant cancer with high lethality rate. In this study, we identify that terminal Uridylyl Transferase 1 (TUT1), a specific terminal uridylyltransferase for U6 snRNA, is required for survival of PDAC, but not for that of normal adult pancreas. Mechanistically, TUT1 uridylylation activity promotes tri-snRNP assembly though facilitating the binding of LSM protein to U6 snRNA. TUT1 deletion leads to global alternative splicing (AS) changes which in turn triggers PDAC cell cycle dysregulation. Here, we reveal a novel function of TUT1 in regulating AS by modulating tri-snRNP levels and identify TUT1 as a potential therapeutic target for the treatment of PDAC.
Published in
Targeting TUT1 Depletes Tri-snRNP Pools to Suppress Splicing and Inhibit Pancreatic Cancer Cell Survival
Guo Z, Huang J, Lu ZJ et al. · Cancer research 2025 · PMID 39854320 · doi:10.1158/0008-5472.CAN-24-2563
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Also filed as BioProject PRJNA875680 and SRA study SRP395215. Searching any of these in the dataset finder brings you back here.

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