Further understanding of the molecular mechanisms responsible for prostate cancer (CaP) development and progression is paramount for overcoming the current diagnostic and therapeutic hurdles presented by this urologic disease. The beta-catenin nuclear signaling molecule has been widely implicated as an oncogene in human cancer, including CaP. Pooling together knowledge gathered on the contributions of beta-catenin and other factors to human neoplasia may assist in the development of better strategies for management and treatment of prostate tumors of all stages (early, advanced/androgen-dependent, advanced/androgen-independent). Although there is considerable lack of comprehension regarding the function of beta-catenin transcriptional activity in prostate tumors in vivo, recent evidence indicates the probability that beta-catenin contributes to multiple signaling pathways for which a causative role in CaP is already known. In this review, we will approach such pathway interactions, perhaps the most notable being androgen receptor (AR) signaling, in order to highlight those avenues through which beta-catenin may exert its cancer-related function. To the same end, we will draw attention to normal beta-catenin signaling in the prostate; however, as only very limited knowledge exists on this topic, much of the discussion will be correlative. Our final topic will concentrate on how, given realistic scenarios of androgen stimulation or absence in both normal and neoplastic prostate cells, nuclear beta-catenin may ultimately potentiate wnt cell-cell signaling and AR activities. Heightening our comprehension of beta-catenin signaling mechanisms and its phenotypic consequences in CaP - and in normal prostate - may contribute to that body of knowledge which will eventually prove useful for devising more effective therapies.

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