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PRMT1 promotes pancreatic cancer development and resistance to chemotherapy

GSE223133 Homo sapiens Genome binding/occupancy profiling by high throughput sequencing 4 samples Submitted 2024/03/09 Platform GPL20795
Summary
Pancreatic ductal adenocarcinoma (PDAC) remains one of the most lethal types of cancer, and novel treatment regimens are direly needed. Epigenetic regulation contributes to the development of various cancer types, but its role in the development of, and potential as a therapeutic target for, PDAC remains underexplored. Here, we show that PRMT1 is highly expressed in murine and human pancreatic cancer and is essential for cancer cell proliferation and tumorigenesis. Deletion of PRMT1 delays pancreatic cancer development in a KRAS-dependent mouse model, and multi-omics analyses reveal that the PRMT1 depletion leads to global changes in chromatin accessibility and transcription, resulting in reduced glycolysis and a decrease in tumorigenic capacity. Pharmacological inhibition of PRMT1 in combination with gemcitabine has a synergistic effect on pancreatic tumor growth in vitro and in vivo. Collectively, our findings implicate PRMT1 as a key regulator of pancreatic cancer development and a promising target for combination therapy.
Published in
PRMT1 promotes pancreatic cancer development and resistance to chemotherapy
Ku B, Eisenbarth D, Baek S et al. · Cell reports. Medicine 2024 · PMID 38460517 · doi:10.1016/j.xcrm.2024.101461
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Also filed as BioProject PRJNA925121 and SRA study SRP418094. Searching any of these in the dataset finder brings you back here.

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