Abstract # D121 Lycopene and astaxanthin inhibit human prostate cancer cell proliferation induced by androgens. Yoav Sharoni, Lilach Agemy, Udit Giat, Elena Kirilov, Michael Danilenko and Joseph Levy, Ben-Gurion University, Beer-Sheva, Israel. Androgens are the classic risk factors and mitogens for prostate cancer. Our aim was to find whether active dietary ingredients such as carotenoids inhibit basal and hormone-stimulated cancer cell growth and to establish a molecular mechanism for their action. Astaxanthin and lycopene inhibited prostate cancer cell proliferation in a dose-dependent manner. Foreskin human fibroblasts were less sensitive to carotenoid inhibition. Dihydrotestosterone (DHT), the active male sex hormone, stimulated cell growth and secretion of prostate specific antigen (PSA) in hormone-dependent (LNCaP), but not in hormone-independent (DU-145) prostate cancer cells. Both lycopene and astaxanthin inhibited the androgen-induced cell proliferation and decreased PSA secretion by ~25% while intracellular PSA level decreased by ~50%. Addition of DHT to LNCaP cells, activated cell cycle progression from G1 to S phase in control cells while the majority of the DHT- and carotenoid-treated cells remained in G1 phase. DHT stimulation of the control cells resulted in an increase in the level of cyclin D1, the key regulator of G0/G1 to S transition. The retinoblastoma (pRb) tumor suppressor protein level and the ratio of its inactive (hyperphosphorylated) form to the active (hypo-phosphorylated) form increased. These changes were significantly attenuated and delayed by lycopene or astaxanthin treatment, concomitantly with an increase in the level of the universal cyclin dependent kinase inhibitor p27kip1. The inhibition of cell growth by the carotenoids was not accompanied by necrosis, as measured either by LDH leakage from or trypan blue uptake by the cells. Moreover, this treatment did not cause apoptotic cell death, as measured by the appearance of sub-G1 peak or poly(ADP-ribose) polymerase (PARP) cleavage. These results provide an explanation for the anticancer activity of a carotenoid-rich diet. The mechanism of this protection is related to reduction in the mitogenic activity of androgens. #B216 This is second-hand smoke. Remember we are NOT Doctors and have NO medical training. This site is like an Encylopedia - there are many pages, many links on many topics. Support our work with any size DONATION - see left side of any page - for how to donate. You can help raise awareness of CAM.