From what I have read E2 is the primary culprit in prostate cancer. High E2 in and low testosterone cause an inbalance that allows the prostate to grow and eventually become cancerous. As you said the role of DHT is a bit tricky. Here is Dinoiii's respond to my question about the role of DHT and the prostate.
"DHT has been wrongfully accused of being the genesis of all things, prostate and hair related, gone wrong.
I am going to simplify things (hopefully not over-simplify)...
Many things are required for upregulation of DHT receptors - perhaps most important in the aformentioned pathologies is the combined product of IGF-1 and Estradiol (E2) at the level of prostatic and hair follicular membranes. Low levels of IGF-1 or E2, low DHT receptor concentration, little effect.
Feed the system DHT (either exogenously or through the amplification pathway), you will get downregulation of said receptors. Come at it from the opposite direction and, like virtually everything else in endocrinology and metabolism, and you get a sort-of negative feedback (the same thing happens with androgens, though the theories have been heatedly contested).
What we do know is that emphasis has since shifted in prostate/follicular therapeutics with greater success with the use of Aromatase Inhibitors (Letrozole) than 5-Alpha Reductase Inhibitors (Fina, Saw Palmetto). Both items will help, however, attacking estrogen is continually more effective or more complete than with blockade of DHT."
D_