GEOapplication/xmlftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE154nnn/GSE154509/primaryOK200OtherHomo sapiensOtherhttps://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE154509GEOGSEfalseLncRNA-NFYB axis drives immune suppression to promote HCC progression by a positive feedbackMetastases 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.2026/07/01GSE154509GSM4672355GSM4672354GSM467235616956154509Homo sapiens[42368565]