{"database":"GEO","file_versions":[{"headers":{"Content-Type":["application/json"]},"body":{"files":{"Other":["ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE303nnn/GSE303307/"]},"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=GSE303307"],"repository":["GEO"],"entry_type":["GSE"],"additional_accession":[]},"is_claimable":false,"name":"Super-enhancer-driven TCF4 promotes neuroblastoma metastasis by mediating GM3 synthesis [RNA-Seq]","description":"Metastasis remains a critical factor for survival in neuroblastoma (NB). Although NB metastasis involves multifaceted regulatory mechanisms, the role of epitranscriptomic regulation in this process has not been elucidated. Here, we identify super-enhancer-driven transcription factor TCF4 as a central orchestrator of metastatic networks in NB, promoting both in vitro and in vivo dissemination. Mechanistically, TCF4 transcriptionally activates SPTLC1, a pivotal enzyme in sphingolipid biosynthesis, to promote ganglioside GM3 synthesis. GM3 orchestrates membrane architecture remodeling, thereby modulating ITGB1 membrame localization and activation, which subsequently potentiates metastasis-associated FAK signaling. Notably, we demonstrate that the HDAC6 inhibitor ACY-1215 suppresses NB malignancy by destabilizing TCF4 protein. These findings reveal an epitranscriptomic-metabolic axis governing NB metastasis and propose ACY-1215 as a translational therapeutic candidate for clinical intervention.","dates":{"publication":"2026/05/27"},"accession":"GSE303307","cross_references":{"GSM":["GSM9123111","GSM9123114","GSM9123115","GSM9123112","GSM9123113","GSM9123118","GSM9123116","GSM9123117"],"GPL":["29480"],"GSE":["303307"],"taxon":["Homo sapiens"],"PMID":["[41630015]"]}}