Anticancer activity of green tea polyphenols in prostate gland

Abstract

Numerous evidences from prevention studies in humans, support the existence of an association between green tea polyphenols consumption and a reduced cancer risk. Prostate cancer is one of the most frequently diagnosed male neoplasia in the Western countries, which is in agreement with this gland being particularly vulnerable to oxidative stress processes, often associated with tumorigenesis. Tea polyphenols have been extensively studied in cell culture and animal models where they inhibited tumor onset and progression. Prostate cancer appears a suitable target for primary prevention care, since it grows slowly, before symptoms arise, thus offering a relatively long time period for therapeutic interventions. It is, in fact, usually diagnosed in men 50-year-old or older, when even a modest delay in progression of the disease could significantly improve the patients quality of life. Although epidemiological studies have not yet yielded conclusive results on the chemopreventive and anticancer effect of tea polyphenols, there is an increasing trend to employ these substances as conservative management for patients diagnosed with less advanced prostate cancer. Here, we intend to review the most recent observations relating tea polyphenols to human prostate cancer risk, in an attempt to outline better their potential employment for preventing prostate cancer.

Figure 1

Chemical structure of the green tea catechins obtained from the dried leaves of the plant Camellia sinensis.

Figure 2

Mechanisms of inhibition of DNMTs by GTCs. (a) In a cancer environment, specific genes are silenced by hypermethylation of their promoters. DNA hypermethylation is catalysed by DNMTs, which use as a substrate SAM and release SAH as a by-product. (b) Within this context GTCs are able to inhibit DNMTs through three distinct mechanisms. (1) Direct inhibition. (2) GTCs are methylated by COMT, resulting in a depletion of SAM and accumulation of the DNMT inhibitor SAH. (3) Direct inhibition of DHFR, resulting in disruption of the folate cycle that influences negatively the levels of SAM. Inhibition of DNMTs ultimately results in DNA hypomethylation and re-expression of previously repressed genes.