The tumor necrosis factor (TNF) receptor RANK (TNFRSF11A) and its ligand RANKL (TNFSF11) regulate osteoclast development and bone metabolism. They also control stem cell expansion and proliferation of mammary epithelial cells via the sex hormone progesterone. As such, RANKL and RANK have been implicated in the onset of hormone-induced breast cancer. Recently, RANK/RANKL were identified as crucial regulators for BRCA1 mutation-driven breast cancer. Current prevention strategies for BRCA1 mutation carriers are associated with wide-ranging risks; therefore, the search for alternative, non-invasive strategies is of paramount importance. We summarize here the functions of the RANKL/RANK pathway in mammalian physiology and focus on its recently uncovered role in breast cancer. We propose that anti-RANKL therapy should be pursued as a preventative strategy for breast cancer.

肿瘤坏死因子（TNF）受体RANK（TNFRSF11A）及其配体RANKL（TNFSF11）调节破骨细胞的发育和骨代谢。它们还通过性激素黄体酮控制干细胞的扩增和乳腺上皮细胞的增殖。因此，RANKL和RANK与激素诱导的乳腺癌的发作有关。最近，RANK / RANKL被确定为BRCA1突变驱动的乳腺癌的关键调节剂。BRCA1的当前预防策略突变携带者与广泛的风险相关；因此，寻找替代的，非侵入性的策略至关重要。我们在这里总结了RANKL / RANK通路在哺乳动物生理中的功能，并着重介绍了其在乳腺癌中最近发现的作用。我们建议应将抗RANKL治疗作为乳腺癌的预防策略。