{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Pan YR"],"funding":["Chang Gung Memorial Hospital, Linkou (Linkou Chang Gung Memorial Hospital)","Chang Gung Memorial Hospital, Linkou"],"pagination":["322-333"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC10874889"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["31(2)"],"pubmed_abstract":["Intrahepatic cholangiocarcinoma (iCCA) is a subtype of CCA and has a high mortality rate and a relatively poor prognosis. However, studies focusing on increased cell motility and loss of epithelial integrity during iCCA progression remain relatively scarce. We collected seven fresh tumor samples from four patients to perform RNA sequencing (RNA-seq) and assay for transposase-accessible chromatin using sequencing (ATAC-seq) to determine the transcriptome profile and chromatin accessibility of iCCA. The increased expression of cell cycle regulators, including PLK1 and its substrate MISP, was identified. Ninety-one iCCA patients were used to validate the clinical significance of PLK1 and MISP. The upregulation of PLK1 and MISP was determined in iCCA tissues. Increased expression of PLK1 and M"],"journal":["Cancer gene therapy"],"pubmed_title":["PLK1 and its substrate MISP facilitate intrahepatic cholangiocarcinoma progression by promoting lymphatic invasion and impairing E-cadherin adherens junctions."],"pmcid":["PMC10874889"],"funding_grant_id":["CORPG3J0251~3","CORPG3L0431~2"],"pubmed_authors":["Pan YR","Yeh CN","Lai JC","Peng PH","Chen CP","Yu AL","Huang WK","Jung SM","Wu CE","Hung TH","Lin SH","Wu KJ"],"additional_accession":[]},"is_claimable":false,"name":"PLK1 and its substrate MISP facilitate intrahepatic cholangiocarcinoma progression by promoting lymphatic invasion and impairing E-cadherin adherens junctions.","description":"Intrahepatic cholangiocarcinoma (iCCA) is a subtype of CCA and has a high mortality rate and a relatively poor prognosis. However, studies focusing on increased cell motility and loss of epithelial integrity during iCCA progression remain relatively scarce. We collected seven fresh tumor samples from four patients to perform RNA sequencing (RNA-seq) and assay for transposase-accessible chromatin using sequencing (ATAC-seq) to determine the transcriptome profile and chromatin accessibility of iCCA. The increased expression of cell cycle regulators, including PLK1 and its substrate MISP, was identified. Ninety-one iCCA patients were used to validate the clinical significance of PLK1 and MISP. The upregulation of PLK1 and MISP was determined in iCCA tissues. Increased expression of PLK1 and M","dates":{"release":"2024-01-01T00:00:00Z","publication":"2024 Feb","modification":"2026-06-09T07:06:22.225Z","creation":"2025-04-05T23:49:23.374Z"},"accession":"S-EPMC10874889","cross_references":{"pubmed":["38057358"],"doi":["10.1038/s41417-023-00705-z"]}}