AURKB as a Therapeutic Target and Key Driver of Liver Cancer Growth and Metastasis

Abstract

Hepatocellular carcinoma (HCC) is a major cause of cancer-related deaths worldwide. Aurora kinase B (AURKB), a critical regulator of mitosis, has been implicated in cancer progression, though its precise role in HCC remains unclear. In this study, AURKB expression was found to be significantly elevated in HCC tissues and cell lines compared to controls, as validated by GEPIA and ENCORI databases. Functional assays revealed that AURKB knockdown reduced cell proliferation, invasion, and migration, while increasing apoptosis. Furthermore, suppression of AURKB affected epithelial-mesenchymal transition (EMT) markers, decreasing vimentin and N-cadherin levels and increasing E-cadherin expression. In vivo, a xenograft mouse model demonstrated that tumors derived from AURKB-silenced cells exhibited reduced growth and fewer lung metastases. Histological and immunohistochemical analyses showed lower levels of Ki-67, MMP-9, and EMT markers in these tumors, alongside increased E-cadherin. These findings highlight AURKB's critical role in promoting HCC progression, metastasis, and EMT regulation. Overexpression of AURKB was associated with poor prognosis, suggesting it could serve as a potential biomarker and therapeutic target for liver cancer. Overall, targeting AURKB may provide a novel approach to inhibit HCC growth and metastasis, improving patient outcomes.