RANK/RANKL expression in prostate cancer

Bone is the most common metastatic site in patients with rostate cancer. Skeletal-related events consisting of pathological racture, spinal cord compression, and intractable pain are causes f a reduced quality of life for patients [1,2]. Denosumab (XGEVA), human monoclonal antibody against receptor activator of nuclear actor kappa B ligand (RANKL), was found to be a new therapeutic ption for bone metastasis [3–5]. Prostate cancer cells penetrate the bone marrow and induce steoblasts to produce cytokines that promote the secretion of ANKL. RANKL expression acceleration induces osteoclast hyperlasia and facilitates bone resorption [1]. Denosumab controls hese mechanisms by inhibiting RANK. A previous study demontrated that primary prostate cancer cells expressed the RANK and ANKL genes, which was further elevated in bone metastasis lesions 6–10]. Therefore, denosumab is expected to exert its antitumor ffect by inhibiting RANKL.