Irisin Induces Apoptosis in Metastatic Prostate Cancer Cells and Inhibits Tumor Growth In Vivo

Background: Prostate cancer is the second most common cancer in males worldwide, with alpha V beta 5 in-tegrin, a coactivator receptor, being highly expressed in advanced prostate cancer. Irisin, a hormone secreted from skeletal muscles, can reduce cell viability and migration and potentially inhibit alpha V beta 5. Objective: This study investigates the potential impact of irisin on prostate cancer cells and its underlying mechanism. Methods: In vitro evaluation of the antiproliferative action of irisin on metastatic prostate cancer (PC-3) cells was tested through MTT assay, flow cytometry, and Western blot. An in vivo evaluation of the antiproliferative effect on prostate cancer xenograft was evaluated in nude mice. Results: In vitro evaluations showed that irisin reduced PC-3 cell viability to 70% and increased the Annexin-V/7AAD positive cell population. Irisin altered the expression of apoptotic proteins, alpha V beta 5, and proteins involved in the P13k-Akt pathway. In vivo, irisin inhibited tumor growth and progression, positively affecting animal well-being. In conclusion, irisin has an apoptotic effect on PC-3, possibly through altering alpha V beta 5 and the Bcl2/BAX and P13k-Akt signaling pathway, inhibiting tumor growth in vivo. Conclusion: Our findings can serve as a foundation for further evaluation of irisin's role in prostate cancer.