The following is an abstract of a paper which, in my opinion, is the
most important research ever done on prostate cancer.  It is well worth
reading the entire article, not just the abstract.

Ed Friedman

The Journal of Clinical Endocrinology & Metabolism Vol. 90, No. 2 893-903
Copyright © 2005 by The Endocrine Society

Membrane Androgen Receptor Activation Induces Apoptotic Regression of
Human Prostate Cancer Cells in Vitro and in Vivo

Anastassia Hatzoglou1, Marilena Kampa1, Christina Kogia1, Ioannis
Charalampopoulos, Panayiotis A. Theodoropoulos, Ploutarchos Anezinis,
Constantina Dambaki, Evangelia A. Papakonstanti, Efstathios N.
Stathopoulos, Christos Stournaras, Achille Gravanis and Elias Castanas

Departments of Experimental Endocrinology (A.., M.K., C.K., E.C.),
Pharmacology (I.C., A.G.), Biochemistry (P.A.T., E.A.P., C.S.), Urology
(P.A.), and Pathology (C.D., E.N.S.), University of Crete School of
Medicine, Heraklion GR-71110, Greece

Nongenomic androgen actions imply mechanisms different from the
classical intracellular androgen receptor (iAR) activation. We have
recently reported the identification of a membrane androgen receptor
(mAR) on LNCaP human prostate cancer cells, mediating testosterone
signal transduction within minutes. In the present study we provide
evidence that activation of mAR by nonpermeable, BSA-coupled
testosterone results in 1) inhibition of LNCaP cell growth (with a 50%
inhibitory concentration of 5.08 nM, similar to the affinity of
testosterone for membrane sites); 2) induction in LNCaP cells of
both apoptosis and the proapoptotic Fas protein; and 3) a significant
decrease in migration, adhesion, and invasion of iAR-negative DU145
human prostate cancer cells. These actions persisted in the presence of
antiandrogen flutamide or after decreasing the content of iAR in LNCaP
cells by iAR antisense oligonucleotides. Testosterone-BSA was also
effective in inducing apoptosis of DU145 human prostate cancer cells,
negative for iAR, but expressing mAR sites. In LNCaP cell-inoculated
nude mice, treatment with testosterone-BSA (4.8 mg/kg body weight) for 1
month resulted in a 60% reduction of tumor size compared with that in
control animals receiving only BSA, an effect that was not affected by
the antiandrogen flutamide. Our findings suggest that activators of mAR
may represent a new class of antitumoral agents of prostate cancer.