Numerous studies have demonstrated that the calcitonin receptor (CALCR) is a specific marker of osteoclast differentiation and that calcitonin can inhibit bone resorption in vitro and in vivo. Mice lacking calcitonin and calcitonin gene-related peptide (CGRP) have a high bone mass phenotype due to an increase in bone formation parameters. Expression of calcitonin (CT) and its receptor (CTR) generate survival, adhesion, pro-inflammatory, and pro-metastatic pathways. Moreover, data indicate a pivotal role for CT-CTR axis in advanced prostate cancer PC metastasis and may serve as a potential therapeutic target for advanced PC.