AURKB drives aggressive phenotype and clinicopathological progression in cholangiocarcinoma

This study aimed to explore the role of AURKB (Aurora kinase B) in the progression of cholangiocarcinoma and evaluate its correlation with pathological characteristics, survival, and cellular function.

We used immunohistochemistry, qRT-PCR, Western blot, CCK-8 cell proliferation assay, scratch assay, colony formation assay, Transwell cell migration assay, lentiviral overexpression and shRNA-mediated knockdown with validation of modulation efficiency, and subcutaneous xenograft tumor model to study the function of AURKB in cholangiocarcinoma. We also collected patients' pathological data, including pathological grade and age, to analyze the correlation with AURKB gene expression.

There were significant differences in the expression of AURKB genes between different pathological grades and age groups. There is a positive correlation with pathological grade, indicating that as the malignancy of the tumor increases, the expression of the AURKB gene also increases. There is a negative correlation with age, indicating that the expression of the AURKB gene decreases as patients age. High expression of the AURKB gene is associated with significantly shortened overall survival in patients with cholangiocarcinoma. The results of the CCK-8 cell proliferation experiment showed that after infection with AURKB lentivirus, the proliferation rate of HCCC-9810 cells significantly increased, while the proliferation rate of HUCCT1 cells significantly decreased. Flow cytometry results showed that in the AURKB high expression group, the apoptosis percentage of HCCC-9810 cells was significantly reduced, while in the AURKB low expression group, the apoptosis percentage of HUCCT1 cells was significantly increased. The results of the colony formation experiment showed that in the AURKB high expression group, the number of clones of HCCC-9810 cells increased significantly, while in the AURKB low expression group, the number of HUCCT1 cell clones did not change significantly. The results of scratch assay and Transwell cell migration assay showed that in the AURKB high-expression group, the migration and invasion abilities of cells were significantly enhanced, while in the AURKB low-expression group, these abilities were weakened. Xenograft tumor experiments showed that AURKB significantly promoted tumor growth.

AURKB plays a key role in the progression of cholangiocarcinoma, and its high expression is associated with increased tumor malignancy, shortened survival, and enhanced cell function. Therefore, AURKB may become a potential therapeutic target for cholangiocarcinoma and provide a new research direction.