<HashMap><database>GEO</database><file_versions><headers><Content-Type>application/xml</Content-Type></headers><body><files><Other>ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE324nnn/GSE324984/</Other></files><type>primary</type></body><statusCode>OK</statusCode><statusCodeValue>200</statusCodeValue></file_versions><scores/><additional><omics_type>Transcriptomics</omics_type><species>Homo sapiens</species><gds_type>Expression profiling by high throughput sequencing</gds_type><full_dataset_link>https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE324984</full_dataset_link><repository>GEO</repository><entry_type>GSE</entry_type></additional><is_claimable>false</is_claimable><name>A MYC Family Switch: L-MYC Drives and Maintains Neuroendocrine Lineage Programs in Prostate Cancer</name><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.</description><dates><publication>2026/05/12</publication></dates><accession>GSE324984</accession><cross_references><GSM>GSM9589989</GSM><GSM>GSM9589988</GSM><GSM>GSM9589992</GSM><GSM>GSM9589993</GSM><GSM>GSM9589994</GSM><GSM>GSM9589995</GSM><GSM>GSM9589990</GSM><GSM>GSM9589991</GSM><GPL>34284</GPL><GSE>324984</GSE><taxon>Homo sapiens</taxon><PMID>[42001796]</PMID></cross_references></HashMap>