2. Academic Validation
  3. AURKB targets DHX9 to promote hepatocellular carcinoma progression via PI3K/AKT/mTOR pathway

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

  • Mol Carcinog. 2024 Jun 14. doi: 10.1002/mc.23775.
Guoqing Zhu 1 2,  Laihui Luo 2,  Yongzhu He 2 3 4,  Yongqiang Xiao 2,  Ziwei Cai 2,  Weilai Tong 5,  Wei Deng 2,  Jin Xie 2,  Yanxin Zhong 5,  Zhigao Hu 2,  Renfeng Shan 2
Affiliations

Affiliations

  • 1 Department of General Surgery, The First Hospital of Nanchang, The Third Affiliated Hospital of Nanchang University, Nanchang, Jiangxi Province, China.
  • 2 Department of General Surgery, The First Affiliated Hospital of Nanchang University, Nanchang, Jiangxi Province, China.
  • 3 Department of General Surgery, Division of Hepatobiliary and Pancreas Surgery, Shenzhen People's Hospital, The Second Clinical Medical College, Jinan University, Shenzhen, Guangdong Province, China.
  • 4 The First Affiliated Hospital, Southern University of Science and Technology, Shenzhen, Guangdong Province, China.
  • 5 Department of Orthopedics, The First Affiliated Hospital of Nanchang University, Nanchang, Jiangxi Province, China.
PMID: 38874176 DOI: 10.1002/mc.23775
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.

Keywords

AURKB; DHX9; HCC; PI3K/AKT/mTOR pathway; protein interaction.

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