Epidemiological evidence strongly suggests that lycopene consumption contributes to prostate cancer risk reduction. Preclinical studies show that lycopene acts via different mechanisms, which have the potential to cooperate in reducing the proliferation of normal and cancerous prostate epithelial cells, in reducing DNA damage, and in improving oxidative stress defense. The mechanisms include inhibition of prostatic IGF-I signaling, IL-6 expression, and androgen signaling. Moreover, lycopene improves gap-junctional communication and induces phase II drug metabolizing enzymes as well as oxidative defense genes. These findings provide plausible explanations for the epidemiological findings how lycopene can contribute to reduced prostate cancer risk. The novel finding that lycopene reduces local androgen signaling in the prostate suggests also efficacy in prevention of benign prostate hyperplasia. Intervention trials in humans are required to finally prove clinical efficacy of the lycopene molecule in prostate health.