BUB1B Promotes Ovarian Cancer Cell Proliferation and Metastasis by Activating the Wnt/β-Catenin Pathway.

BACKGROUND: BUB1 mitotic checkpoint serine/threonine kinase B (BUB1B) has been found to participate in cancer progression. Nevertheless, the function and mechanism of BUB1B in ovarian cancer (OC) remain unknown. METHOD: Based on datasets GSE14407, GSE18520, and the TCGA combined GTEx database, the differently expressed genes (DEGs) between OC tissues and para-carcinoma tissues were identified. These DEGs were subjected to protein-protein interaction analysis to obtain hub genes, with BUB1B serving as a candidate for further study. Subsequently, the prognostic value was analyzed. To elucidate the role of BUB1B, knockdown experiments were conducted in vitro and in vivo to assess alterations in malignant behaviors, while β-catenin expression was quantified by qRT-PCR and western blot. Moreover, the Wnt/β-catenin pathway inhibitor LGK974 was utilized to demonstrate whether the effects of BUB1B are mediated by the Wnt/β-catenin pathway. RESULTS: High BUB1B expression was observed in OC tissues and cell lines, and it was identified as a hub DEG with prognostic value in OC. Following BUB1B knockdown, cell proliferation, migration, invasion, and tumor growth and metastasis were suppressed in vitro and in vivo. Mechanically, BUB1B knockdown inhibited the expression of β-catenin and inactivated the Wnt/β-catenin pathway. In addition, BUB1B overexpression promoted the malignant behavior of OC cells, which was inhibited by LGK974. CONCLUSION: BUB1B is an oncogene whose expression level is negatively correlated with the prognosis of OC patients. Mechanically, BUB1B promotes the progression of OC via the Wnt/β-catenin pathway. Our study offers a potential therapeutic target for OC treatment.