Journal article
Role of osteoprotegerin (OPG) in cancer.
- Abstract:
- OPG (osteoprotegerin), a secreted member of the TNF (tumour necrosis factor) receptor superfamily, has a variety of biological functions which include the regulation of bone turnover. OPG is a potent inhibitor of osteoclastic bone resorption and has been investigated as a potential therapeutic for the treatment of both osteoporosis and tumour-induced bone disease. Indeed, in murine models of cancer-induced bone disease, inhibition of osteoclastic activity by OPG was also associated with a reduction in tumour burden. The discovery that OPG can bind to and inhibit the activity of TRAIL (TNF-related apoptosis-inducing ligand) triggered extensive research into the potential role of OPG in the regulation of tumour cell survival. A number of reports from studies using in vitro models have shown that OPG protects tumour cells from the effects of TRAIL, thereby possibly providing tumour cells that produce OPG with a survival advantage. However, the ability of OPG to act as a tumour cell survival factor remains to be verified using appropriate in vivo systems. A third area of interest has been the use of OPG as a prognostic marker in various cancer types, including myeloma, breast and prostate cancer. This review provides an overview of the role of OPG in cancer, both in cancer-induced bone disease and in tumour growth and survival.
- Publication status:
- Published
Actions
Access Document
- Publisher copy:
- 10.1042/cs20050175
Authors
- Journal:
- Clinical science (London, England : 1979) More from this journal
- Volume:
- 110
- Issue:
- 3
- Pages:
- 279-291
- Publication date:
- 2006-03-01
- DOI:
- EISSN:
-
1470-8736
- ISSN:
-
0143-5221
- Language:
-
English
- Keywords:
- Pubs id:
-
pubs:384068
- UUID:
-
uuid:f3cf3dfd-bc95-46a0-998b-19d501084757
- Local pid:
-
pubs:384068
- Source identifiers:
-
384068
- Deposit date:
-
2013-11-16
- ARK identifier:
Terms of use
- Copyright date:
- 2006
If you are the owner of this record, you can report an update to it here: Report update to this record