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AURKB activates EMT through PI3K/AKT signaling axis to promote ICC progression
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 th...
Autores principales: | , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Springer US
2023
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10272048/ https://www.ncbi.nlm.nih.gov/pubmed/37318676 http://dx.doi.org/10.1007/s12672-023-00707-1 |
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author | Ma, Peng Hao, Ying Wang, Wei Zhang, Yue-Feng Yu, Kai-Huan Wang, Wei-Xing |
author_facet | Ma, Peng Hao, Ying Wang, Wei Zhang, Yue-Feng Yu, Kai-Huan Wang, Wei-Xing |
author_sort | Ma, Peng |
collection | PubMed |
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. Importantly, we discovered that AURKB regulates the expressions of EMT-related genes via PI3K/AKT signaling axis. Herein, our results suggest that AURKB induced EMT through the activation of PI3K/AKT signaling pathway is critical to the progression of ICC, which may be a prospective therapeutic treatment for overcoming ICC metastasis and progression. SUPPLEMENTARY INFORMATION: The online version contains supplementary material available at 10.1007/s12672-023-00707-1. |
format | Online Article Text |
id | pubmed-10272048 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2023 |
publisher | Springer US |
record_format | MEDLINE/PubMed |
spelling | pubmed-102720482023-06-17 AURKB activates EMT through PI3K/AKT signaling axis to promote ICC progression Ma, Peng Hao, Ying Wang, Wei Zhang, Yue-Feng Yu, Kai-Huan Wang, Wei-Xing Discov Oncol Research 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. Importantly, we discovered that AURKB regulates the expressions of EMT-related genes via PI3K/AKT signaling axis. Herein, our results suggest that AURKB induced EMT through the activation of PI3K/AKT signaling pathway is critical to the progression of ICC, which may be a prospective therapeutic treatment for overcoming ICC metastasis and progression. SUPPLEMENTARY INFORMATION: The online version contains supplementary material available at 10.1007/s12672-023-00707-1. Springer US 2023-06-15 /pmc/articles/PMC10272048/ /pubmed/37318676 http://dx.doi.org/10.1007/s12672-023-00707-1 Text en © The Author(s) 2023 https://creativecommons.org/licenses/by/4.0/Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this licence, visit http://creativecommons.org/licenses/by/4.0/ (https://creativecommons.org/licenses/by/4.0/) . |
spellingShingle | Research Ma, Peng Hao, Ying Wang, Wei Zhang, Yue-Feng Yu, Kai-Huan Wang, Wei-Xing AURKB activates EMT through PI3K/AKT signaling axis to promote ICC progression |
title | AURKB activates EMT through PI3K/AKT signaling axis to promote ICC progression |
title_full | AURKB activates EMT through PI3K/AKT signaling axis to promote ICC progression |
title_fullStr | AURKB activates EMT through PI3K/AKT signaling axis to promote ICC progression |
title_full_unstemmed | AURKB activates EMT through PI3K/AKT signaling axis to promote ICC progression |
title_short | AURKB activates EMT through PI3K/AKT signaling axis to promote ICC progression |
title_sort | aurkb activates emt through pi3k/akt signaling axis to promote icc progression |
topic | Research |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10272048/ https://www.ncbi.nlm.nih.gov/pubmed/37318676 http://dx.doi.org/10.1007/s12672-023-00707-1 |
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