作者: Yohei Sekino , Naohide Oue , Shoichiro Mukai , Yoshinori Shigematsu , Keisuke Goto
DOI: 10.1002/PROS.23728
关键词:
摘要: Background Prostate cancer (PCa) is a common malignancy worldwide and the second leading cause of death in men. The standard therapy for advanced PCa androgen deprivation (ADT). Although ADT, including bicalutamide treatment, initially effective, resistance to frequently occurs leads development castration-resistant PCa. Thus, clarifying mechanisms urgently needed. We designed this study assess expression function PCDHB9, which encodes protocadherin B9 protein. Methods PCDHB9 was determined using immunohistochemistry qRT-PCR. effects overexpression or knockdown on cell growth, migration, adhesion were evaluated. To evaluate PCDHB9-mediated PCa, we performed gene analysis DU145 transfected with PCDHB9. examined inhibition resistance. Results qRT-PCR revealed that much higher than non-neoplastic prostate tissues. In 152 clinically localized cases showed 59% positive B9. A Kaplan-Meier high associated PSA recurrence after radical prostatectomy. functional modulated migration adhesion. also found induced ITGB6 based analysis. effect sensitivity MTT assays. IC50 value siRNA-transfected cells significantly lower negative control cells. Furthermore, immunohistochemical staining 74 patients who treated depletion therapy, demonstrated poor overall survival. Conclusions plays an important role progression Collectively, our results suggest targeted may be more effective alone.