Department of General Surgery, The First Hospital of Nanchang, The Third Affiliated Hospital of Nanchang University, Nanchang, Jiangxi Province, China.
Department of General Surgery, The First Affiliated Hospital of Nanchang University, Nanchang, Jiangxi Province, China.
Mol Carcinog. 2024 Sep;63(9):1814-1826. doi: 10.1002/mc.23775. Epub 2024 Jun 14.
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.
极光激酶 B（AURKB）在多种癌症中发挥致癌作用，但在肝癌中的潜在机制尚不清楚。本研究旨在探讨 AURKB 在肝细胞癌（HCC）中的作用及其潜在的分子机制。生物信息学分析显示，AURKB 在 HCC 组织和细胞系中显著过表达，其高表达与 HCC 患者的预后不良相关。此外，下调 AURKB 抑制 HCC 细胞增殖、迁移和侵袭，诱导细胞凋亡，并导致细胞周期停滞。此外，AURKB 的下调还抑制了 HCC 的肺转移。AURKB 与 DExH-Box 解旋酶 9（DHX9）相互作用，并靶向 HCC 细胞中的表达。挽救实验进一步表明，AURKB 通过靶向 DHX9 促进 HCC 进展，是通过 PI3K/AKT/mTOR 通路实现的。我们的研究结果表明，AURKB 在 HCC 中表达显著升高，与患者的预后相关。AURKB 通过靶向 DHX9 促进 HCC 进展是通过 PI3K/AKT/mTOR 通路实现的。
