{"database":"GEO","file_versions":[{"headers":{"Content-Type":["application/json"]},"body":{"files":{"Other":["ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE336nnn/GSE336546/"]},"type":"primary"},"statusCodeValue":200,"statusCode":"OK"}],"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=GSE336546"],"repository":["GEO"],"entry_type":["GSE"],"additional_accession":[]},"is_claimable":false,"name":"CpG Hypermethylation and WNT/AP-1 cooperativity Define the Epigenetic Landscape and a Clinical Subgroup of High-Risk Pediatric Adrenocortical Carcinoma [cell line]","description":"Treatment of two adult ACC cell lines (H295R and CU-ACC1) with the HDAC inhibitor entinostat led to consistent dose-dependent reductions in viability, outperforming the DNA demethylating agent decitabine. scRNA-seq analyses revealed global transcriptional reprogramming. This included downregulation of AP-1 transcription factors (FOS, JUND, JUNB), suppression of oxidative phosphorylation and steroidogenic pathways, and increased expression of pro-apoptotic genes. These findings support entinostat's potential to reverse high-risk epigenetic programs in pACT and highlight HDAC inhibition as a promising therapeutic avenue, particularly when combined with established treatments.","dates":{"publication":"2026/08/12"},"accession":"GSE336546","cross_references":{"GSM":["GSM9837159","GSM9837158","GSM9837160","GSM9837157","GSM9837156","GSM9837155"],"GPL":["34284"],"GSE":["336546"],"taxon":["Homo sapiens"],"PMID":["[42736301]"]}}