Transcriptomic analysis reveals AURKB promotes malignant progression of hepatocellular carcinoma

Due to the poor prognosis of hepatocellular carcinoma (HCC), there is an urgent need to identify novel therapeutic targets. This study aims to evaluate the potential of Aurora kinase B (AURKB) as a therapeutic target for HCC and provide a theoretical basis for immunotherapy in HCC. In this study, 374 patients were included from The Cancer Genome Atlas (TCGA) database, and single-sample gene set enrichment analysis was performed to classify them into high-immunity and low-immunity groups. Through differential gene expression analysis and univariate Cox regression analysis, AURKB was screened out as a risk gene, followed by Kaplan-Meier survival analysis, immune infiltration analysis, and pathway enrichment analysis. The results demonstrated that overexpression of AURKB was associated with worse overall survival (OS) and disease-free survival (DFS) in HCC patients. High AURKB expression was correlated with increased infiltration of CD8 + T cells, macrophages, and dendritic cells, along with elevated expression of immune checkpoint molecules, including programmed death-1 (PD-1), cytotoxic T lymphocyte-associated antigen-4 (CTLA-4), CD80, and CD86. To further validate the role of AURKB in HCC, we constructed HCC cell lines with AURKB knockdown. Knockdown of AURKB inhibited HCC cell proliferation, colony formation, migration, and invasion. Functional experiments further indicate that AURKB promotes CD8 + T cell exhaustion and immune evasion. In conclusion, our study indicates that AURKB is an immune-related prognostic biomarker that promotes immune escape and tumor progression in HCC.