{"database":"GEO","file_versions":[{"headers":{"Content-Type":["application/json"]},"body":{"files":{"Other":["ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE346nnn/GSE346902/"]},"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=GSE346902"],"repository":["GEO"],"entry_type":["GSE"],"additional_accession":[]},"is_claimable":false,"name":"Combinatorial E2F knockdown in the prostate cancer PM154 cell line","description":"Treatment-emergent neuroendocrine prostate cancer (CRPC-NE) arises through RB1 loss and lineage plasticity in response to androgen receptor-targeted therapies, creating constitutive E2F transcription factor addiction that lacks effective therapeutic exploitation. All six E2F family members harbour a conserved U12-type minor intron within their dimerisation domain — processed exclusively by the minor spliceosome — creating a single post-transcriptional node whose inhibition simultaneously targets the entire activator E2F programme. Combinatorial E2F knockdown RNA-seq revealed E2F3 as the dominant activator E2F and uncovered a paradoxical dual role for the E2F family as gatekeepers of neuroendocrine identity — complete E2F depletion unleashing an ASCL1-driven differentiation programme resembling pancreatic beta cell specification.","dates":{"publication":"2026/09/11"},"accession":"GSE346902","cross_references":{"GSM":["GSM10042291","GSM10042292","GSM10042293","GSM10042294","GSM10042290","GSM10042299","GSM10042288","GSM10042300","GSM10042289","GSM10042301","GSM10042302","GSM10042295","GSM10042284","GSM10042296","GSM10042285","GSM10042297","GSM10042286","GSM10042287","GSM10042298","GSM10042307","GSM10042303","GSM10042304","GSM10042305","GSM10042306"],"GPL":["24676"],"GSE":["346902"],"taxon":["Homo sapiens"]}}