<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Ma P</submitter><funding>Opening Project of Hubei Key Laboratory</funding><pagination>102</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC10272048</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>14(1)</volume><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</pubmed_abstract><journal>Discover. Oncology</journal><pubmed_title>AURKB activates EMT through PI3K/AKT signaling axis to promote ICC progression.</pubmed_title><pmcid>PMC10272048</pmcid><funding_grant_id>2021KFY007</funding_grant_id><pubmed_authors>Ma P</pubmed_authors><pubmed_authors>Zhang YF</pubmed_authors><pubmed_authors>Wang W</pubmed_authors><pubmed_authors>Yu KH</pubmed_authors><pubmed_authors>Hao Y</pubmed_authors><pubmed_authors>Wang WX</pubmed_authors></additional><is_claimable>false</is_claimable><name>AURKB activates EMT through PI3K/AKT signaling axis to promote ICC progression.</name><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</description><dates><release>2023-01-01T00:00:00Z</release><publication>2023 Jun</publication><modification>2025-04-22T01:58:02.729Z</modification><creation>2025-04-05T20:14:10.822Z</creation></dates><accession>S-EPMC10272048</accession><cross_references><pubmed>37318676</pubmed><doi>10.1007/s12672-023-00707-1</doi></cross_references></HashMap>