{"database":"GEO","file_versions":[{"headers":{"Content-Type":["application/json"]},"body":{"files":{"Other":["ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE270nnn/GSE270157/"]},"type":"primary"},"statusCode":"OK","statusCodeValue":200}],"scores":null,"additional":{"omics_type":["Genomics"],"species":["Homo sapiens"],"gds_type":["Genome binding/occupancy profiling by high throughput sequencing"],"full_dataset_link":["https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE270157"],"repository":["GEO"],"entry_type":["GSE"],"additional_accession":[]},"is_claimable":false,"name":"Linker histone variant H1-10 promotes prostate cancer proliferation [ChIP-seq]","description":"While the linker histone H1 is recognized for its role in stabilizing higher-order chromatin structures, the distinct functions of its variants remain underexplored. In this study, we uncover that the H1-10 is markedly overexpressed in prostate cancer and associates with a poor prognosis. H1-10 is mainly localized to the nucleolus, where it facilitates nucleolar assembly through liquid condensation. H1-10 amplifies ribosomal RNA (rRNA) transcription by directly associating with RNA polymerase I (Pol I), thereby enhancing Pol I binding affinity for ribosomal DNA (rDNA). This results in expanded production of rRNA and elevated global protein translation. By further investigation, we found that H1-10 boosts the protein translation of transcription factor E2F3, which in turn induces the transcription of cell growth genes by increasing the level of CTD serine 5 phosphorylated RNA polymerase II at gene promoters. Critically, through high-throughput virtual screening, we identified specific small molecules that inhibit H1-10 by targeting its DNA binding domain. On-target validations showed these molecules blocked H1-10-mediated Pol I rDNA occupancy, global protein translation and prostate tumor growth in vitro and in vivo. In summary, our study reveals the critical role of H1-10 in ribosome biogenesis and prostate cancer progression, and pioneers the pharmacological targeting of an H1 variant, highlighting the therapeutic promise of targeting histone variants.","dates":{"publication":"2026/05/06"},"accession":"GSE270157","cross_references":{"GSM":["GSM8335695","GSM8335684","GSM8335685","GSM8335696","GSM8335697","GSM8335686","GSM8335698","GSM8335687","GSM8335691","GSM8335692","GSM8335693","GSM8335683","GSM8335694","GSM8335703","GSM8335704","GSM8335688","GSM8335699","GSM8335700","GSM8335689","GSM8335701","GSM8335702","GSM8335690"],"GPL":["24676","34284"],"GSE":["270157"],"taxon":["Homo sapiens"]}}