{"database":"GEO","file_versions":[{"headers":{"Content-Type":["application/json"]},"body":{"files":{"Other":["ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE324nnn/GSE324984/"]},"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=GSE324984"],"repository":["GEO"],"entry_type":["GSE"],"additional_accession":[]},"is_claimable":false,"name":"A MYC Family Switch: L-MYC Drives and Maintains Neuroendocrine Lineage Programs in Prostate Cancer","description":"Neuroendocrine prostate cancer (NEPC) is an aggressive and therapy-resistant subtype that emerges through lineage plasticity following inhibition of the androgen receptor (AR) signaling pathway. In this study, MYCL was overexpressed in prostate adenocarcinoma C4-2B cells and knocked down in neuroendocrine prostate cancer NCI-H660 cells to investigate its role in lineage regulation. RNA-sequencing analysis revealed that MYCL overexpression suppresses AR signaling and MYC target signaling while inducing neuroendocrine-like transcriptional reprogramming. In contrast, MYCL knockdown disrupts neuroendocrine lineage identity and restores adenocarcinoma-associated gene expression programs, including reactivation of MYC. These findings suggest that MYCL plays a key role in regulating lineage plasticity and maintaining neuroendocrine transcriptional programs in prostate cancer.","dates":{"publication":"2026/05/12"},"accession":"GSE324984","cross_references":{"GSM":["GSM9589989","GSM9589988","GSM9589992","GSM9589993","GSM9589994","GSM9589995","GSM9589990","GSM9589991"],"GPL":["34284"],"GSE":["324984"],"taxon":["Homo sapiens"],"PMID":["[42001796]"]}}