Working model for the interaction of AR and Wnt/β-Catenin signaling pathway in castration-resistant prostate cancer cells. In normal conditions, Wnt and androgen signaling function at different cell populations (A&B). In prostate cancer where both pathways may be deregulated in the same cells, androgens may inhibit the input of AR into the Wnt signaling pathway where β-Catenin can potentiate the AR signaling (C). In castration-resistant prostate cancer cells, Wnt can activate both signaling pathways turning the unliganded AR into a coactivator of the Wnt dependent transcriptional program (D).
Schweizer et al. BMC Cell Biology 2008 9:4 doi:10.1186/1471-2121-9-4