Secreted frizzled-related protein 5 suppresses aggressive phenotype and reverses docetaxel resistance in prostate cancer.

摘要: Secreted frizzled-related protein 5 (SFRP5) has been reported to be downregulated in prostate cancer. However, its biological role this malignancy not clarified yet. In the present study, we performed SFRP5 overexpression experiments determine function cancer cell growth, invasion, tumorigenesis, and docetaxel sensitivity. Our results showed that of significantly suppressed proliferation colony formation PC-3 DU-145 cells, compared with vector-transfected control cells. arrested cells at G0/G1 phase induced apoptosis. Transwell invasion assay revealed ectopic expression inhibited Overexpression resensitized docetaxel-resistant docetaxel, which was coupled increased Mechanistically, blocked β-catenin nuclear translocation transcriptional activity. vivo studies confirmed growth xenograft tumors. SFRP5-transfected tumors a reduction percentage Ki-67-positive proliferating an increase terminal deoxynucleotidyl transferasebiotin-dUTP nick end labeling-positive These data suggest suppresses aggressive phenotype overcomes resistance through inactivation signaling. Therefore, delivery may offer therapeutic benefits treatment