{"database":"GEO","file_versions":[{"headers":{"Content-Type":["application/json"]},"body":{"files":{"Other":["ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE154nnn/GSE154509/"]},"type":"primary"},"statusCode":"OK","statusCodeValue":200}],"scores":null,"additional":{"omics_type":["Other"],"species":["Homo sapiens"],"gds_type":["Other"],"full_dataset_link":["https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE154509"],"repository":["GEO"],"entry_type":["GSE"],"additional_accession":[]},"is_claimable":false,"name":"LncRNA-NFYB axis drives immune suppression to promote HCC progression by a positive feedback","description":"Metastases are the main cause of cancer mortality, but the mechanisms underlying aggressive progression remain poorly understood. Genome-wide characterization of chromatin accessibility reveals the opening of large numbers of distal regulatory elements across the genome during metastatic progression, which correlate with NFYB. Further, hepatocellular LINC01137 mitigates antitumour T cell responses by expanding MDSC to promote HCC metastasis via stabilizing NFYB to recruit SMYD3 to upregulate IL-1β, CXCL2 and CCL20. Mechanistically, LINC01137 recruits SMYD3 to increase the occupancy of H3K4me3 on promoters of IL-1β, CXCL2 and CCL20 by NFYB. Importantly, LINC01137 transcription is activated by NFYB/KAT2B complex in a feed-forward loop. Clinically, Concordant overexpression of LINC01137-NFYB and MDSC markers positively correlates with poorer survival. Notably, IL-1β inhibitor enhances the blockade efficacy of PD-L1 in LINC01137-overexpressing HCC. Our results delineate an immunosuppressive mechanism of LINC01137-NFYB signalling during HCC progression and supply a proof for the concept of engineering microenvironment in HCC immunotherapy.","dates":{"publication":"2026/07/01"},"accession":"GSE154509","cross_references":{"GSM":["GSM4672355","GSM4672354","GSM4672356"],"GPL":["16956"],"GSE":["154509"],"taxon":["Homo sapiens"],"PMID":["[42368565]"]}}