Background: Prostate cancer remains one of the most common and deadliest forms of cancer, generally
respond well to radical prostatectomy and associated interventions, up to 30% of individuals will suffer
disease relapse. Although BUB1B was found to be essential for cell growth and proliferation, even in several
kinds of tumor cells, the specific importance and mechanistic role of BUB1B in prostate cancer remain unclear.
Methods: Quantitative Real-Time PCR and Western-blot were used in the detection of mRNA and protein expression.
Lentivirus infection was used to overexpression or knock down the target gene. Flow cytometry analysis
was performed to test protein expression and apoptosis level. Immunohistochemistry was used to identify
protein expression in tissue. Statistical differences between the two groups are evaluated by two-tailed t-tests.
The comparison among multiple groups is performed by one-way Analysis of Variance (ANOVA) followed by
Dunnett’s posttest. The statistical significance of the Kaplan-Meier survival plot is determined by log-rank
Results: In the present report, we found BUB1B expression to be highly increased in prostate cancer tissues
relative to normal controls. We further found BUB1B to be essential for efficient tumor cell proliferation, and to
correlate with poorer prostate cancer patient outcomes. From a mechanistic perspective, the ability of BUB1B to
regulate MELK was found to be essential for its ability to promote prostate cancer cell proliferation.
Conclusion: Altogether, our data suggest that BUB1B is up-regulated in prostate cancer, suggesting that the
growth of cancer cells may depend on BUB1B-dependent regulation of MELK transcription. BUB1B may serve
as a clinical prognostic factor and a druggable target for prostate cancer.