Fili Sofia, Karalaki Maria, Schaller Bernhard
Medical School, National and Kapodistrian University of Athens, 75 Micras Asias, Goudi-Athens, 115 27, Greece.
Cancer Lett. 2009 Sep 28;283(1):10-9. doi: 10.1016/j.canlet.2009.01.011. Epub 2009 Feb 6.
Osteoprotegerin (OPG), member of tumor necrosis factor (TNF) receptor superfamily, has various biological functions including bone remodeling. OPG binds to receptor activator of nuclear factor-kB ligand (RANKL) and prevents osteoclastic bone resorption. Recently, OPG has gained more clinical interest as its role in cancer-mediated bone destruction and the potential of RANKL inhibition could act as a novel treatment in tumor-induced bone disease. OPG protects prostate cancer cells from apoptotic effects of TRAIL and therefore provides tumor cells producing OPG with survival advantages. Additionally, the increased RANKL/OPG ratio in metastatic breast cancer results in severe osteolysis. Thus, bone formation and resorption are the crux of cancer metastasis, resulting in bone pain and pathological fractures. This review provides an overview of the role of OPG in cancer-induced bone disease.
骨保护素（OPG）是肿瘤坏死因子（TNF）受体超家族成员，具有包括骨重塑在内的多种生物学功能。OPG与核因子-κB受体激活剂配体（RANKL）结合，阻止破骨细胞介导的骨吸收。近来，OPG因其在癌症介导的骨破坏中的作用以及RANKL抑制的潜力可能成为肿瘤诱导性骨病的一种新治疗方法而受到更多临床关注。OPG保护前列腺癌细胞免受TRAIL的凋亡作用，因此为产生OPG的肿瘤细胞提供生存优势。此外，转移性乳腺癌中RANKL/OPG比值增加会导致严重的骨溶解。因此，骨形成和骨吸收是癌症转移的关键，会导致骨痛和病理性骨折。本综述概述了OPG在癌症诱导性骨病中的作用。
