{"database":"GEO","file_versions":[{"headers":{"Content-Type":["application/json"]},"body":{"files":{"Txt":["ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE336nnn/GSE336205/suppl/GSE336205_genes_fpkm_expression.txt.gz"],"Other":["ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE336nnn/GSE336205/"]},"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=GSE336205"],"repository":["GEO"],"entry_type":["GSE"],"additional_accession":[]},"is_claimable":false,"name":"DUSP5 regulates ferroptosis in pancreatic cancer by down-regulating SCD1 expression via ERK1/2","description":"This study aimed to explore the role and mechanism of DUSP5 in pancreatic ductal adenocarcinoma (PDAC). RNA sequencing was performed in DUSP5-overexpressing PANC-1 cells and control cells to identify differentially expressed genes. The results revealed that DUSP5 significantly downregulated stearoyl-CoA desaturase 1 (SCD1), a key enzyme involved in fatty acid metabolism and ferroptosis regulation. Our findings indicate that DUSP5 promotes ferroptosis and suppresses PDAC proliferation through the ERK1/2-SCD1 signaling pathway.","dates":{"publication":"2026/06/28"},"accession":"GSE336205","cross_references":{"GSM":["GSM9829997","GSM9829998","GSM9829995","GSM9829996","GSM9829993","GSM9829994"],"GPL":["24676"],"GSE":["336205"],"taxon":["Homo sapiens"]}}