Observational studies and prevention trials suggested that selenium supplement was effective in reducing the incidence and mortality of prostate cancer. Bone metastases are the most advanced complications in many cancers including prostate cancer and they are incurable. We previously demonstrated that selenium disrupts androgen and estrogen receptor signalings in prostate cancer and breast cancer cells. In this study, we investigated the effect of selenium on bone metastasis through affecting the bone remodeling process in SaOS-2 B10 cell. Selenium inhibited the transcription activity of receptor activator of NF-kappaB ligand (RANKL) with the use of a RANKL promoter luciferase construct. Selenium significantly down-regulated the mRNA levels of osteocalcin, RUNX2 and osteoprotegerin in a dose dependent manner by northern blot. Interestingly, the mRNA level of bone morphogenic protein 4 (BMP 4) was not affected by selenium. Furthermore, selenium inhibited the cell growth and reduced the alkaline phosphatase activity of SaOS-2 B10 cell. This study will contribute towards a better understanding of the chemopreventive action of selenium and may provide a rationale for selenium intervention in bone metastasis.

98th AACR Annual Meeting-- Apr 14-18, 2007; Los Angeles, CA