Osteoprotegerin inhibits prostate cancer-induced osteoclastogenesis and prevents prostate tumor growth in the bone.

@article{Zhang2001OsteoprotegerinIP,
  title={Osteoprotegerin inhibits prostate cancer-induced osteoclastogenesis and prevents prostate tumor growth in the bone.},
  author={Jun Zhang and Jie Dai and Ying Qi and Din Lii Lin and P Smith and C L Strayhorn and Akiko Mizokami and Zheng Fu and Jacob Westman and Evan T. Keller},
  journal={The Journal of clinical investigation},
  year={2001},
  volume={107 10},
  pages={
          1235-44
        }
}
Prostate cancer (CaP) forms osteoblastic skeletal metastases with an underlying osteoclastic component. However, the importance of osteoclastogenesis in the development of CaP skeletal lesions is unknown. In the present study, we demonstrate that CaP cells directly induce osteoclastogenesis from osteoclast precursors in the absence of underlying stroma in vitro. CaP cells produced a soluble form of receptor activator of NF-kappaB ligand (RANKL), which accounted for the CaP-mediated… Expand
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The findings indicate that prostate cancer mediates osteoclastogenesis through induction of RANKL expression by osteoblasts and through direct actions on osteOClast precursors mediated by some factors other than RankL. Expand
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TLDR
The molecular mechanisms underlying the direct osteoclastogenic effect of prostate cancer derived factors are revealed, which may be beneficial in developing novel osteoprotegerin-targeting therapeutic approaches. Expand
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TLDR
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TLDR
Study on the pleiotropic functions of RankL in tumorigenesis and metastasis is now expanding beyond the bone field and has been established as one of the most important areas of “ RANKL biology ”. Expand
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TLDR
It is demonstrated that at lower expression rates, tumor-derived OPG enhances the chemotactic RankL gradient and osteolysis, whereas at higher expression rates OPG broadly inhibits RANKL and decreases osteolytic and tumor burden. Expand
Mechanisms of osteoblastic metastases: role of endothelin-1.
TLDR
Evidence is provided that tumor-produced endothelin-1 mediates osteoblastic bone metastases by stimulating osteoblast proliferation and new bone formation and that Endothelin A receptor blockade may be useful for the prevention and treatment of osteoblasts attributable to breast or prostate cancer. Expand
Monocyte chemotactic protein-1 mediates prostate cancer-induced bone resorption.
TLDR
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