{"database":"GEO","file_versions":[{"headers":{"Content-Type":["application/json"]},"body":{"files":{"Other":["ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE333nnn/GSE333210/"]},"type":"primary"},"statusCode":"OK","statusCodeValue":200}],"scores":null,"additional":{"omics_type":["Transcriptomics"],"species":["Homo sapiens"],"gds_type":["Expression profiling by high throughput sequencing"],"full_dataset_link":["https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE333210"],"repository":["GEO"],"entry_type":["GSE"],"additional_accession":[]},"is_claimable":false,"name":"ZEB1 K80R Suppresses the NF-κB/EMT Axis and Tumor Pro-inflammatory Gene Expression","description":"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.","dates":{"publication":"2026/05/30"},"accession":"GSE333210","cross_references":{"GSM":["GSM9759197","GSM9759195","GSM9759196"],"GPL":["34284"],"GSE":["333210"],"taxon":["Homo sapiens"]}}