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AURKB targets DHX9 to promote hepatocellular carcinoma progression via PI3K/AKT/mTOR pathway.

Authors :
Zhu G
Luo L
He Y
Xiao Y
Cai Z
Tong W
Deng W
Xie J
Zhong Y
Hu Z
Shan R
Source :
Molecular carcinogenesis [Mol Carcinog] 2024 Sep; Vol. 63 (9), pp. 1814-1826. Date of Electronic Publication: 2024 Jun 14.
Publication Year :
2024

Abstract

Aurora kinase B (AURKB) is known to play a carcinogenic role in a variety of cancers, but its underlying mechanism in liver cancer is unknown. This study aimed to investigate the role of AURKB in hepatocellular carcinoma (HCC) and its underlying molecular mechanism. Bioinformatics analysis revealed that AURKB was significantly overexpressed in HCC tissues and cell lines, and its high expression was associated with a poorer prognosis in HCC patients. Furthermore, downregulation of AURKB inhibited HCC cell proliferation, migration, and invasion, induced apoptosis, and caused cell cycle arrest. Moreover, AURKB downregulation also inhibited lung metastasis of HCC. AURKB interacted with DExH-Box helicase 9 (DHX9) and targeted its expression in HCC cells. Rescue experiments further demonstrated that AURKB targeting DHX9 promoted HCC progression through the PI3K/AKT/mTOR pathway. Our results suggest that AURKB is significantly highly expressed in HCC and correlates with patient prognosis. Targeting DHX9 with AURKB promotes HCC progression via the PI3K/AKT/mTOR pathway.<br /> (© 2024 The Author(s). Molecular Carcinogenesis published by Wiley Periodicals LLC.)

Details

Language :
English
ISSN :
1098-2744
Volume :
63
Issue :
9
Database :
MEDLINE
Journal :
Molecular carcinogenesis
Publication Type :
Academic Journal
Accession number :
38874176
Full Text :
https://doi.org/10.1002/mc.23775