{"database":"GEO","file_versions":[{"headers":{"Content-Type":["application/json"]},"body":{"files":{"Other":["ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE346nnn/GSE346317/"]},"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=GSE346317"],"repository":["GEO"],"entry_type":["GSE"],"additional_accession":[]},"is_claimable":false,"name":"FUT3-dependent DDX21 fucosylation links elevated CA19-9 to pancreatic cancer metastasis via MIB2 alternative splicing and E-cadherin destabilization","description":"Elevated carbohydrate antigen 19-9 (CA19-9) is strongly associated with distant metastasis and poor prognosis in pancreatic ductal adenocarcinoma (PDAC), yet the underlying mechanisms remain unclear. In this study, we investigated a FUT3-dependent glycosylation–splicing regulatory mechanism involved in pancreatic cancer metastasis. RNA sequencing was performed in BxPC-3 pancreatic cancer cells with DDX21 overexpression and corresponding vector controls to characterize DDX21-dependent transcriptional and alternative splicing changes. Integrated analyses identified MIB2 exon 8 skipping as a functionally relevant downstream event associated with E-cadherin destabilization and metastatic phenotypes.","dates":{"publication":"2026/09/12"},"accession":"GSE346317","cross_references":{"GSM":["GSM10031881","GSM10031880","GSM10031879","GSM10031876","GSM10031878","GSM10031877"],"GPL":["24676"],"GSE":["346317"],"taxon":["Homo sapiens"]}}