Lycopene Effects Contributing to Prostate Health

Abstract

Epidemiological evidence links lycopene consumption with decreased prostate cancer risk. Several signaling pathways have been identified as players in prostate cancer development. Chronic prostatitis, for example, due to infections, is a suggested risk factor for prostate cancer. Endogenous production of reactive oxygen species during inflammation may lead to oxidative DNA damage, which can be mutagenic, if unrepaired. Androgen signaling, cytokine (IL-6, IL-4) and growth factor signaling (e.g., IGF, Wnt/β-catenin) cross-talk via PI3K/Akt, MAPK, and Jak/STAT pathways have been identified as major controllers of prostate growth. During disease progression, and after androgen ablation therapy, the remaining operational pathways are upregulated to compensate for the lost growth signal, finally resulting in androgen-independent prostate cancer. Lycopene modulates several of the aforementioned pathways, providing a promising rationale for prostate cancer risk reduction by lycopene: In many experimental setups, lycopene reduced inflammatory signals, prevented oxidative DNA damage, modulated the expression or activity of IGF axis members, of Wnt/β-catenin and androgen signalling, and enhanced gap junctional communication. Lycopene's influence on these pathways likely contributes to the observed cell growth inhibition and apoptosis induction by lycopene. A substantial part of the lycopene effects can be explained by its antioxidant action, but other mechanisms might also be involved.