Prostate cancer is initially dependent on androgens for growth; hence, recurrent 
prostate is treated with androgen ablation which may result in progression to 
androgen independence characterized by a resistance to such therapy. Androgens 
bind to and activate the androgen receptor (AR), a member of the nuclear steroid 
receptor family of transcription factors, which regulates prostate cancer cell 
proliferation and survival in androgen-independent, as well as -dependent, 
tumors. Another pathway regulating proliferation and survival is the 
phosphatidylinositol 3-kinase (PI3K)/Akt pathway. Here we analyze reports in the 
literature indicating that these two pathways cooperate to regulate prostate 
tumor development and progression. Studies show that AR transcriptional activity 
and expression are regulated by Akt. In addition, androgens regulate the Akt 
pathway by both genomic and non-genomic effects. This explains why prostate 
tumors subjected to androgen ablation experience an increase in Akt 
phosphorylation, and suggest that the tumor compensates for the loss of one 
pathway with another. Different modes of interaction between the two pathways, 
including direct interaction, or regulation via downstream intermediates, such 
as the wnt/GSK-3beta/beta-catenin pathway, NF-kappaB, and the FOXO family of 
transcription factors, will be discussed. In addition, we will discuss the role 
of Akt in the interaction of the AR with upstream regulators of Akt 
phosphorylation, such as receptor tyrosine kinases of the EGF and IGF-1 receptor 
families and the tumor suppressor PTEN.