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ZEB1 K80R Suppresses the NF-κB/EMT Axis and Tumor Pro-inflammatory Gene Expression

GSE333210 Homo sapiens Expression profiling by high throughput sequencing 3 samples Submitted 2026/05/30 Platform GPL34284
Summary
This study demonstrates that ZEB1 K80 is a critical lysine residue acetylated by p300. Deacetylation of ZEB1 at K80 (K80R mutation) significantly suppresses the epithelial-mesenchymal transition (EMT) program and the expression of tumor inflammation-related genes, leading to downregulation of EMT markers (e.g., VIM, MMP9) and pro-inflammatory cytokines/chemokines (e.g., ICAM1, CCL5, CXCL8, CSF2, TNFα). Pathway enrichment analysis reveals that NF-κB signaling, inflammatory response, and EMT-related pathways are markedly inhibited. Collectively, our data provide key molecular insights into the role of ZEB1 acetylation in tumor progression: deacetylation at the K80 site of ZEB1 significantly attenuates tumor cell proliferation and metastasis.
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Also filed as BioProject PRJNA1470498 and SRA study SRP703614. Searching any of these in the dataset finder brings you back here.

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