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

ABSTRACT: 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.

ORGANISM(S): Homo sapiens

PROVIDER: GSE333210 | GEO | 2026/05/30

REPOSITORIES: GEO