<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/GSE346nnn/GSE346317/</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=GSE346317</full_dataset_link><repository>GEO</repository><entry_type>GSE</entry_type></additional><is_claimable>false</is_claimable><name>FUT3-dependent DDX21 fucosylation links elevated CA19-9 to pancreatic cancer metastasis via MIB2 alternative splicing and E-cadherin destabilization</name><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.</description><dates><publication>2026/09/12</publication></dates><accession>GSE346317</accession><cross_references><GSM>GSM10031881</GSM><GSM>GSM10031880</GSM><GSM>GSM10031879</GSM><GSM>GSM10031876</GSM><GSM>GSM10031878</GSM><GSM>GSM10031877</GSM><GPL>24676</GPL><GSE>346317</GSE><taxon>Homo sapiens</taxon></cross_references></HashMap>