{"database":"GEO","file_versions":[{"headers":{"Content-Type":["application/json"]},"body":{"files":{"Other":["ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE344nnn/GSE344391/"]},"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=GSE344391"],"repository":["GEO"],"entry_type":["GSE"],"additional_accession":[]},"is_claimable":false,"name":"PRCC-TFE3 Forms Proline-dependent Condensates and Reprograms Chromatin for tRCC Oncogenic Transcription [ATAC-seq]","description":"Translocation renal cell carcinoma (tRCC) is an aggressive malignancy driven by MiT/TFE family transcription factor rearrangements, most notably TFE3 fusions. Among these, the PRCC::TFE3 fusion is a prominent oncogenic driver, yet the molecular mechanisms governing its transcriptional and tumorigenic activities remain poorly defined. Here, we demonstrate that PRCC::TFE3 forms dynamic, transcriptionally active nuclear condensates that are critical for its oncogenic function. We identify a proline-rich region within the PRCC fusion partner as the essential determinant of condensate formation. Disruption of this proline-rich region (PRW) abolishes condensate assembly, reverses fusion-driven chromatin accessibility and transcriptional reprogramming, and suppresses proliferative, migratory, and invasive phenotypes in patient-derived tRCC cell lines. Integrative RNA-seq, ATAC-seq, and CUT&RUN analyses reveal that PRCC::TFE3 condensates function as epigenetic regulatory hubs, coordinating extensive chromatin remodeling and recruitment of transcription factor networks—including TEAD-associated pathways—to amplify oncogenic programs. Furthermore, we identify HS3ST2 and ABCB5 as novel, condensate-dependent target genes and validate them as critical mediators of tRCC progression. Our findings establish PRCC::TFE3-mediated condensate formation as a fundamental mechanism of tRCC pathogenesis and highlight condensate-dependent transcriptional networks as potential therapeutic vulnerabilities in this clinically challenging disease.","dates":{"publication":"2026/08/20"},"accession":"GSE344391","cross_references":{"GSM":["GSM9978322","GSM9978311","GSM9978321","GSM9978324","GSM9978313","GSM9978312","GSM9978323","GSM9978315","GSM9978325","GSM9978314","GSM9978317","GSM9978316","GSM9978319","GSM9978318","GSM9978320"],"GPL":["34284"],"GSE":["344391"],"taxon":["Homo sapiens"]}}