[High expression of MYBL2 promotes progression and predicts a poor survival outcome of prostate cancer].

OBJECTIVE

To explore the correlation of MYB proto-oncogene like 2 (MYBL2) with biological behaviors and clinical prognosis of prostate cancer (PCa).

METHODS

We detected Mybl2 mRNA expression in 45 pairs of PCa and adjacent tissues using real-time quantitative PCR, and analyzed the correlation of high (23 cases) and low expression (22 cases) of with clinicopathological features and prognosis of the patients using nonparametric test, Kaplan-Meier survival analysis and univariate and multivariate Cox regression. The results were verified by analysis of the data from Cancer Genome Atlas (TCGA) microarray database, and the molecular pathways were identified by gene set enrichment analysis (GSEA). The CIBERPORT algorithm was used to identify the correlations between expression and tumor microenvironment of PCa. We also tested the effects of MYBL2 knockdown on proliferation and invasion of PCa cell lines using cell counting kit-8 and Transwell assays and observed the growth of PC3 cell xenograft with MYBL2 knockdown in nude mice and the expression levels of Ki-67 in the xenograft using immunohistochemistry.

RESULTS

expression was significantly elevated in PCa tissues in close correlation with Gleason score and clinical and pathological stage of the tumor ( < 0.01) but not with the patients' age. Kaplan-Meier analysis indicated a significant negative correlation of high expression with recurrence-free survival ( < 0.05), but not with the overall survival of the patients. The data from TCGA suggested that clinical and pathological stages were independent prognostic factors for recurrence-free survival, and our data indicated that clinical stage and Gleason score were independent prognostic factors of PCa ( < 0.05). GSEA suggested that expression was related with the pathways involving immune function, cell adhesion, and cytokine secretion; CIBERPORT analysis suggested the involvement of expression with memory B cells and resting mast cells ( < 0.05). In LNCaP and PC-3 cells, MYBL2 knockdown significantly inhibited cell proliferation and invasion ( < 0.05); in the tumor-bearing nude mice, the xenografts derived from PC-3 cells with MYBL2 knockdown exhibited a lowered mean tumor weight and positivity rate for Ki67 ( < 0.05).

CONCLUSION

is an oncogene related with multiple pathological indicators of PCa and can serve as a potential prognostic marker as well as a therapeutic target for patients with PCa.