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Interuption of Klf5 acetylaiton at K358 affects tumor microenvironment in Pten deficient mouse prostates

GSE262893 Mus musculus Expression profiling by high throughput sequencing 4 samples Submitted 2024/06/24 Platform GPL24247
Summary
PTEN deficiency induces KLF5 acetylation; and the interruption of KLF5 acetylation orchestrates intricate interactions between cancer cells and CAFs that enhance FGFR1 signaling and promote tumor growth. Deacetylated KLF5 promotes tumor cells to secrete TNF, which stimulates inflammatory CAFs to release FGF9. Single-cell transcriptomic analysis reveals an enhanced FGF signaling from fibroblasts to cancer cells after the interruption of Klf5 acetylation.
Published in
Interruption of KLF5 acetylation promotes PTEN-deficient prostate cancer progression by reprogramming cancer-associated fibroblasts
Zhang B, Liu M, Mai F et al. · The Journal of clinical investigation 2024 · PMID 38781024 · doi:10.1172/JCI175949
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Also filed as BioProject PRJNA1094424 and SRA study SRP498826. Searching any of these in the dataset finder brings you back here.

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