{"database":"GEO","file_versions":[{"headers":{"Content-Type":["application/json"]},"body":{"files":{"Other":["ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE322nnn/GSE322593/"]},"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=GSE322593"],"repository":["GEO"],"entry_type":["GSE"],"additional_accession":[]},"is_claimable":false,"name":"Context-dependent effects of DHRS2 on cell-cycle progression, apoptosis and inflammatory gene expression in breast cell lines","description":"Basal DHRS2 expression showed significant variation across different cell lines, with the highest levels observed in the non-tumorigenic MCF-10A. Silencing DHRS2 disrupted pathways such as ribosome biogenesis, DNA replication, and ion transport, whereas overexpression altered mitochondrial gene transcription and nucleoside synthesis. Loss of DHRS2 accelerated cell-cycle progression in MCF-7 and MCF-10A cells, whereas its overexpression induced G0/G1 phase arrest. Apoptosis levels increased with knockdown and decreased with overexpression, mainly in cancer cells. Inflammatory gene responses varied depending on cell type, particularly involving CASP1, IL-1A/B, and PYHIN1. Overexpression of DHRS2 promoted cell detachment and migration, suggesting cytoskeletal remodeling.","dates":{"publication":"2026/09/22"},"accession":"GSE322593","cross_references":{"GSM":["GSM9555283","GSM9555284","GSM9555285","GSM9555286","GSM9555287","GSM9555288","GSM9555289","GSM9555278","GSM9555279","GSM9555280","GSM9555281","GSM9555282"],"GPL":["24676"],"GSE":["322593"],"taxon":["Homo sapiens"]}}