Aurora kinase B as a therapeutic target in HPV-induced cervical cancer: mechanisms and future perspectives

Aurora kinase B (AURKB) is a core component of the chromosomal passenger complex, which plays a central role in regulating chromosome condensation, spindle checkpoint function, and cytokinesis. Dysregulated AURKB activity leads to chromosomal instability and aneuploidy, which are the key drivers of oncogenesis. In cervical cancer, persistent infection with high-risk human papillomaviruses (HPV16 and HPV18) initiates carcinogenesis through the viral oncoproteins E6 and E7, which disable tumor suppressor pathways. Recent evidence indicates that E6 and E7 also influence AURKB activity, thereby exacerbating genomic instability, overriding cell-cycle checkpoints, and accelerating tumor progression. Overexpression of AURKB has been reported in cervical cancer and correlated with tumor stage, therapeutic resistance, and poor prognosis. Preclinical investigations demonstrate that pharmacological inhibition of AURKB suppresses tumor cells proliferation, induces mitotic catastrophe, and enhances sensitivity to chemotherapy and radiotherapy. Although clinical evaluation of these AURKB inhibitors such as barasertib (AZD1152) and AZD2811 remains limited, early findings support their potential efficacy, particularly in rationally designed combination regimens. This review describes the mechanistic interplay between HPV oncogenes and AURKB, highlights its role as a biomarker of aggressive disease, and critically assesses the therapeutic promise of AURKB inhibition. Finally, we outline future perspectives on integrating AURKB-targeted therapies into precision oncology for HPV-driven cervical cancer.