Key roles of the OPG-RANK-RANKL system in bone oncology
Osteoprotegerin (OPG)-receptor activator of nuclear factor- B (RANK) and RANK ligand (RANKL) have been identified as members of a ligand-receptor system that directly regulates osteoclast differentiation and osteolysis. RANKL may be a powerful inducer of bone resorption through its interaction with...
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| Veröffentlicht in: | Expert review of anticancer therapy 2007-02, Vol.7 (2), p.221-232 |
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| creator | Baud huin, M Duplomb, L Velasco, C Ruiz Fortun, Y Heymann, D Padrines, M |
| description | Osteoprotegerin (OPG)-receptor activator of nuclear factor- B (RANK) and RANK ligand (RANKL) have been identified as members of a ligand-receptor system that directly regulates osteoclast differentiation and osteolysis. RANKL may be a powerful inducer of bone resorption through its interaction with RANK, and OPG is a soluble decoy receptor that acts as a strong inhibitor of osteoclastic differentiation. Any dysregulation of their respective expression leads to pathological conditions. Furthermore, recent data demonstrate that the OPG-RANK-RANKL system modulates cancer cell migration, thus controlling the development of bone metastases. This review describes the most recent knowledge on the OPG-RANK-RANKL system, its involvement in bone oncology and the new therapeutic approaches based on this molecular triad. |
| doi_str_mv | 10.1586/14737140.7.2.221 |
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RANKL may be a powerful inducer of bone resorption through its interaction with RANK, and OPG is a soluble decoy receptor that acts as a strong inhibitor of osteoclastic differentiation. Any dysregulation of their respective expression leads to pathological conditions. Furthermore, recent data demonstrate that the OPG-RANK-RANKL system modulates cancer cell migration, thus controlling the development of bone metastases. 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RANKL may be a powerful inducer of bone resorption through its interaction with RANK, and OPG is a soluble decoy receptor that acts as a strong inhibitor of osteoclastic differentiation. Any dysregulation of their respective expression leads to pathological conditions. Furthermore, recent data demonstrate that the OPG-RANK-RANKL system modulates cancer cell migration, thus controlling the development of bone metastases. This review describes the most recent knowledge on the OPG-RANK-RANKL system, its involvement in bone oncology and the new therapeutic approaches based on this molecular triad.</description><subject>Animals</subject><subject>bone</subject><subject>Bone cancer</subject><subject>Bone Neoplasms - metabolism</subject><subject>Bone Neoplasms - pathology</subject><subject>Bone Neoplasms - physiopathology</subject><subject>Bone Remodeling - physiology</subject><subject>Bone resorption</subject><subject>Bone Resorption - metabolism</subject><subject>Bone Resorption - pathology</subject><subject>Bone Resorption - physiopathology</subject><subject>Cancer</subject><subject>Cell migration</subject><subject>Data processing</subject><subject>Genetic aspects</subject><subject>Genetic regulation</subject><subject>Humans</subject><subject>Metastases</subject><subject>Oncology</subject><subject>OPG</subject><subject>osteoblast</subject><subject>osteoclast</subject><subject>Osteoclastogenesis</subject><subject>Osteoclasts</subject><subject>Osteoclasts (Biology)</subject><subject>Osteolysis</subject><subject>Osteoprotegerin</subject><subject>Osteoprotegerin - physiology</subject><subject>primary tumor</subject><subject>RANK Ligand - physiology</subject><subject>RANKL</subject><subject>Receptor Activator of Nuclear Factor-kappa B - physiology</subject><subject>Reviews</subject><subject>secondary tumor</subject><subject>TRANCE protein</subject><issn>1473-7140</issn><issn>1744-8328</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2007</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><recordid>eNp9kUFv1DAQhS1ERUvhzglFnHpJsMdJ7MBpVUFBXbUVgrPl2ONuKicudlYo_x5vd1EFEpUle-T53viNh5A3jFaske17VgsuWE0rUUEFwJ6REybqupQc5PMc53S5yx-TlyndUQoN4_CCHDMBUjacnRBxiUsRg8dUBFfMGyyuby7Kb6ury4dtXaQlzTgWw1T0YcIiTCb4cLu8IkdO-4SvD-cp-fH50_fzL-X6-uLr-Wpdmrrr5hI62XGKzjgO2Mq21Uw6a7WWYBswtZZGdLY3EqiVfY_M1YLq7Jtp23XA-Ck529e9j-HnFtOsxiEZ9F5PGLZJMWiEbCSvIaPv_kHvwjZO2Z2SgjYCeMszVO2hW-1RDZMLc9QmL4vjYHKHbsj3KwDeSNrKXVW6F5gYUoro1H0cRh0XxajaDUH9GYISChQ8eH57MLLtR7SPgsOvZ-DjHti9H0f9K0Rv1awXH6KLejJDUvyJ8h_-Um9Q-3ljdMTHhv8r_g2TQ6P7</recordid><startdate>20070201</startdate><enddate>20070201</enddate><creator>Baud huin, M</creator><creator>Duplomb, L</creator><creator>Velasco, C Ruiz</creator><creator>Fortun, Y</creator><creator>Heymann, D</creator><creator>Padrines, M</creator><general>Informa Healthcare</general><general>Taylor & Francis</general><general>Expert Reviews Ltd</general><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>3V.</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8AO</scope><scope>8C1</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>BENPR</scope><scope>CCPQU</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>K9.</scope><scope>M0S</scope><scope>M1P</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>7TO</scope><scope>H94</scope></search><sort><creationdate>20070201</creationdate><title>Key roles of the OPG-RANK-RANKL system in bone oncology</title><author>Baud huin, M ; 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RANKL may be a powerful inducer of bone resorption through its interaction with RANK, and OPG is a soluble decoy receptor that acts as a strong inhibitor of osteoclastic differentiation. Any dysregulation of their respective expression leads to pathological conditions. Furthermore, recent data demonstrate that the OPG-RANK-RANKL system modulates cancer cell migration, thus controlling the development of bone metastases. This review describes the most recent knowledge on the OPG-RANK-RANKL system, its involvement in bone oncology and the new therapeutic approaches based on this molecular triad.</abstract><cop>England</cop><pub>Informa Healthcare</pub><pmid>17288531</pmid><doi>10.1586/14737140.7.2.221</doi><tpages>12</tpages></addata></record> |
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| ispartof | Expert review of anticancer therapy, 2007-02, Vol.7 (2), p.221-232 |
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| subjects | Animals bone Bone cancer Bone Neoplasms - metabolism Bone Neoplasms - pathology Bone Neoplasms - physiopathology Bone Remodeling - physiology Bone resorption Bone Resorption - metabolism Bone Resorption - pathology Bone Resorption - physiopathology Cancer Cell migration Data processing Genetic aspects Genetic regulation Humans Metastases Oncology OPG osteoblast osteoclast Osteoclastogenesis Osteoclasts Osteoclasts (Biology) Osteolysis Osteoprotegerin Osteoprotegerin - physiology primary tumor RANK Ligand - physiology RANKL Receptor Activator of Nuclear Factor-kappa B - physiology Reviews secondary tumor TRANCE protein |
| title | Key roles of the OPG-RANK-RANKL system in bone oncology |
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