Dysregulation of Wnt signalling, a hallmark of which is the stabilization of the transcriptional co-activator β catenin, can lead to several types of cancer, including prostate cancer. Activation of the Wnt/β catenin pathway has effects on prostate cell proliferation, differentiation and the epithelial–mesenchymal transition. In this Review, the authors discuss how the pathway is activated and consider the possible therapeutic application of drugs that target Wnt/β catenin signalling. The Wnts are secreted cysteine-rich glycoproteins that have important roles in the developing embryo as well as in tissue homeostasis in adults. Dysregulation of Wnt signalling can lead to several types of cancer, including prostate cancer. A hallmark of the signalling pathway is the stabilization of the transcriptional co-activator β-catenin, which not only regulates expression of many genes implicated in cancer but is also an essential component of cadherin cell adhesion complexes. β-catenin regulates gene expression by binding members of the T-cell-specific transcription factor/lymphoid enhancer-binding factor 1 (TCF/LEF-1) family of transcription factors. In addition, β-catenin associates with the androgen receptor, a key regulator of prostate growth that drives prostate cancer progression. Wnt/β-catenin signalling can be controlled by secreted Wnt antagonists, many of which are downregulated in cancer. Activation of the Wnt/β-catenin pathway has effects on prostate cell proliferation, differentiation and the epithelial–mesenchymal transition, which is thought to regulate the invasive behaviour of tumour cells. However, whether targeting Wnt/β-catenin signalling is a good therapeutic option for prostate cancer remains unclear.