Department of Biochemistry and Molecular Cell Biology, The Pennsylvania State University, University Park, PA 16802, USA.
Breast Cancer Res. 2010;12(6):215. doi: 10.1186/bcr2781. Epub 2010 Dec 16.
Breast cancer frequently metastasizes to the skeleton, interrupting the normal bone remodeling process and causing bone degradation. Osteolytic lesions are the end result of osteoclast activity; however, osteoclast differentiation and activation are mediated by osteoblast production of RANKL (receptor activator for NFκB ligand) and several osteoclastogenic cytokines. Osteoblasts themselves are negatively affected by cancer cells as evidenced by an increase in apoptosis and a decrease in proteins required for new bone formation. Thus, bone loss is due to both increased activation of osteoclasts and suppression of osteoblasts. This review summarizes the current understanding of the osteolytic mechanisms of bone metastases, including a discussion of current therapies.
乳腺癌常转移至骨骼，打断正常的骨重塑过程，导致骨质降解。破骨细胞活性导致溶骨性病变；然而，破骨细胞分化和激活是由成骨细胞产生的 RANKL（核因子 κB 配体受体激活剂）和几种破骨细胞生成细胞因子介导的。癌细胞也会对成骨细胞产生负面影响，表现为细胞凋亡增加和新骨形成所需蛋白减少。因此，骨质流失既归因于破骨细胞的过度激活，也归因于成骨细胞的抑制。本文综述了骨转移的溶骨性机制的现有认识，包括对现有治疗方法的讨论。
