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...

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Bibliographic Details
Published in:Discover. Oncology 2023-06, Vol.14 (1), p.102-102, Article 102
Main Authors: Ma, Peng, Hao, Ying, Wang, Wei, Zhang, Yue-Feng, Yu, Kai-Huan, Wang, Wei-Xing
Format: Article
Language:English
Subjects:
Antibodies
Cancer Research
Cell cycle
Cell growth
Experiments
Gastric cancer
Infections
Internal Medicine
Kinases
Liver
Lymphatic system
Medical prognosis
Medicine
Medicine & Public Health
Metastasis
Molecular Medicine
Oncology
Prostate cancer
Radiotherapy
Surgical Oncology
Tumors
Wound healing
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Summary: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.
ISSN:2730-6011
2730-6011
DOI:10.1007/s12672-023-00707-1