Background: Prostate cancer is one of the most commonly diagnosed cancers and one of the most
common causes of cancer-related deaths among men worldwide. Patients who are diagnosed with localized
prostate cancer and treated with radical prostatectomy often respond well to therapy. The current standard therapy
for prostate cancer involves maximal surgical resection, followed by radiotherapy and chemotherapy. Clarifying
the molecular mechanism of tumor proliferation and recurrence becomes more and more important for
clinical therapies of prostate cancer.
Methods: Quantitative Real-Time PCR and Western-blot were used in the detection of mRNA and protein expression.
Lentivirus infection was used to overexpress or knockdown 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 this study, we identified that FOXM1 expression was significantly enriched in prostate cancer compared
with normal tissue. Additionally, FOXM1 was functionally required for tumor proliferation and its expression
was associated with poor prognosis in prostate cancer patients. Mechanically, FOXM1-dependent regulation
of EZH2 is essential for proliferation and progression in prostate cancer.
Conclusion: Taken together, our data suggest that oncogenic transcription factor FoxM1 is up-regulated in
prostate cancer, suggesting that the growth of cancer cells may depend on FOXM1 activity. FOXM1 may serve
as a clinical prognostic factor and a therapeutic target for prostate cancer.