GEOapplication/xmlftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE346nnn/GSE346902/primaryOK200TranscriptomicsHomo sapiensExpression profiling by high throughput sequencinghttps://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE346902GEOGSEfalseCombinatorial E2F knockdown in the prostate cancer PM154 cell lineTreatment-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.2026/09/11GSE346902GSM10042291GSM10042292GSM10042293GSM10042294GSM10042290GSM10042299GSM10042288GSM10042300GSM10042289GSM10042301GSM10042302GSM10042295GSM10042284GSM10042296GSM10042285GSM10042286GSM10042297GSM10042287GSM10042298GSM10042307GSM10042303GSM10042304GSM10042305GSM1004230624676346902Homo sapiens