Objective  To clarify the expression level of Aurora-B in drug-resistant ovarian cancer (OC) and its impact on the proliferation, apoptosis, invasion, and migration abilities of OC cisplatin (DPP) resistant cells.

Methods  Immunohistochemistry was used to detect the levels of Aurora-B protein in ovarian tissues from patients with epithelial ovarian cancer (EOC) and uterine fibroids. Overexpression plasmids and siRNA were employed to construct OC drug-resistant cell models with overexpression and knockdown of the Aurora-B gene. The expression levels of Aurora-B protein and mRNA were detected using Western blot and qPCR. CCK-8 assay and EDU experiment were used to assess the proliferation ability of OC cells. Transwell and invasion assays were performed to evaluate the changes in migration and invasion abilities of OC cells. YF 647A-Annexin V/PI dual staining method was used to detect cell apoptosis.

Results  Compared with normal tissues, Aurora-B expression was significantly increased in EOC tissues and further elevated in DDP-resistant tissues (P<0.05). qPCR and Western blot showed that both mRNA and baseline protein levels of Aurora-B were higher in SKOV3/DDP cells than in SKOV3 cells (P<0.05). The CCK-8 assay and EDU proliferation assay demonstrated that Aurora-B upregulation significantly promoted SKOV3 cell proliferation, while Aurora-B knockdown markedly inhibited SKOV3/DDP cell proliferation (P<0.05). Transwell assays revealed that Aurora-B upregulation enhanced the migration and invasion abilities of SKOV3 cells, whereas Aurora-B knockdown reduced these abilities in SKOV3/DDP cells (P<0.05). Apoptosis assays indicated that Aurora-B upregulation suppressed cell apoptosis, while Aurora-B knockdown promoted it.

Conclusion Aurora-B is highly expressed in DDP-resistant OC tissues and cells. High Aurora-B expression enhances OC cell proliferation, invasion, and migration while inhibiting apoptosis. This confirms the promoting role of Aurora-B in drug-resistant OC.

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