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

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.