RANK and c-Met in prostate cancer

Prostate cancer metastasis to bone is lethal and there is no adequate animal model for studying the mechanisms underlying the metastatic process. Here, Chu and colleagues report that receptor activator of NF-κB ligand (RANKL) expressed by prostate cancer cells consistently induced colonization or metastasis to bone in animal models. They went on to establish the mechanism involved, which induces RANKL and c-Met, while repressing androgen receptor (AR) expression and AR signaling pathways. These findings identify a novel mechanism of tumor growth in bone that involves tumor cell reprogramming via RANK–RANKL signaling, as well as a form of signal amplification that mediates recruitment and stable transformation of non-metastatic bystander dormant cells.

Read the full article at Chu et al. (2014) Endocrine-Related Cancer 21 311–326; DOI:10.1530