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Chromatin-occupancy profiling of PRMT5 and METTL3 in prostate cancer cells

GSE217412 Homo sapiens Genome binding/occupancy profiling by high throughput sequencing 6 samples Submitted 2024/09/03 Platform GPL24676
Summary
Prostate cancer (PCa) is the most frequently diagnosed malignancy in men worldwide. Epigenetic regulation has been recognized as a main mechanism of cancer evolution. PRMT5 is the major type II protein arginine methyltransferase catalyzing the symmetric dimethylation of arginine, and METTL3 is the enzymatic component of the large N6-adenosine-methyltransferase complex in mammalian responsible for N6-methyladenosine (m6A) modification in diverse RNA species. Both genes are found upregulated in PCa. However, their exact functional contribution to prostate tumorigenesis is unknown. As both proteins can regulate transcription via binding to chromatin, we seek to explore their DNA binding profiles in both AR+ LNCaP and AR- PC3 cells via recently developed CUT&Tag technique. Antibodies we used were Active Motif #61001 for PRMT5 and Abcam #195352 for METTL3. Our data suggests that both proteins regulate PCa cell biology, at least partially, through chromatin-binding and subsequent transcriptional regulation. CUT&Tag assay for arginine methyltransferase PRMT5 and N6‐adenosine‐methyltransferase METTL3 in LNCaP and PC3 cells
Published in
Inhibition of PRMT5 moderately suppresses prostate cancer growth in vivo but enhances its response to immunotherapy
He Q, Zhang Y, Li W et al. · Cancer letters 2024 · PMID 39218291 · doi:10.1016/j.canlet.2024.217214
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Also filed as BioProject PRJNA898967 and SRA study SRP406589. Searching any of these in the dataset finder brings you back here.

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