{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Ma P"],"funding":["Opening Project of Hubei Key Laboratory"],"pagination":["102"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC10272048"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["14(1)"],"pubmed_abstract":["Intrahepatic cholangiocarcinoma (ICC) is a fatal disease and the molecular mechanism of its progression remains unknown. Aurora Kinase B (AURKB) is a central regulator of chromosome separation and cytokinesis and is abnormally expressed in a variety of cancer cells. This research aimed to explore the effect of AURKB in occurrence and metastasis of ICC. We found that AURKB showed a progressive up-regulation pattern from normal bile duct tissue to ICC with high invasion. Our data showed that AURKB significantly promoted ICC cell proliferation, induced epithelial-mesenchymal transition (EMT), migration and invasion through gain- and loss- of function experiments. In vivo results consistently showed that AURKB up-regulation not only promoted tumor growth, but also promoted tumor metastasis. Im"],"journal":["Discover. Oncology"],"pubmed_title":["AURKB activates EMT through PI3K/AKT signaling axis to promote ICC progression."],"pmcid":["PMC10272048"],"funding_grant_id":["2021KFY007"],"pubmed_authors":["Ma P","Zhang YF","Wang W","Yu KH","Hao Y","Wang WX"],"additional_accession":[]},"is_claimable":false,"name":"AURKB activates EMT through PI3K/AKT signaling axis to promote ICC progression.","description":"Intrahepatic cholangiocarcinoma (ICC) is a fatal disease and the molecular mechanism of its progression remains unknown. Aurora Kinase B (AURKB) is a central regulator of chromosome separation and cytokinesis and is abnormally expressed in a variety of cancer cells. This research aimed to explore the effect of AURKB in occurrence and metastasis of ICC. We found that AURKB showed a progressive up-regulation pattern from normal bile duct tissue to ICC with high invasion. Our data showed that AURKB significantly promoted ICC cell proliferation, induced epithelial-mesenchymal transition (EMT), migration and invasion through gain- and loss- of function experiments. In vivo results consistently showed that AURKB up-regulation not only promoted tumor growth, but also promoted tumor metastasis. Im","dates":{"release":"2023-01-01T00:00:00Z","publication":"2023 Jun","modification":"2025-04-22T01:58:02.729Z","creation":"2025-04-05T20:14:10.822Z"},"accession":"S-EPMC10272048","cross_references":{"pubmed":["37318676"],"doi":["10.1007/s12672-023-00707-1"]}}