Peiminine suppresses prostate cancer progression by regulating cell proliferation, motility, apoptosis, and mitochondrial dysfunction.

BACKGROUND: Peiminine, an active alkaloid, has been reported to exhibit antitumor properties in several malignancies. This study aims to examine the role and potential mechanism of peiminine in prostate cancer (PCa). METHODS: CCK-8, wound healing, colony formation, and Transwell assays were employed to evaluate PCa cell phenotypes. Cell cycle progression and apoptosis were examined by flow cytometry. Mitochondrial ROS, mitochondrial membrane potential, and ATP levels were measured to evaluate mitochondrial function in PCa cells. Western blotting was used to assess protein levels associated with apoptosis, EMT, and Wnt/β-catenin signaling. Immunofluorescence staining was performed to detect β-catenin expression. The in vivo effects of peiminine were evaluated using a xenograft mouse model. RESULTS: Peiminine dose-dependently impaired PCa cell viability without significantly affecting non-tumor cells. Peiminine inhibited PCa cell growth and motion and triggered apoptosis, cell cycle arrest, and mitochondrial dysfunction in vitro. Peiminine reduced PCa cell-derived tumor growth in the xenograft mouse model. Peiminine inhibited Wnt/β-catenin signal transduction. CONCLUSION: Peiminine exhibits an antitumor role in PCa by targeting Wnt/β-catenin signaling.