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Androgens and their receptors are crucial factors contributing to PCa development, growth, and progression [82]. Treatment of androgen-dependent (LNCaP) and androgen-independent (LNCaP-AR and DU145) human PCa cell lines with PFE and PJ displayed decreased expression of genes involved in androgen biosynthesis, such as 3β-hydroxysteroid dehydrogenase type 2, aldo-keto reductase family 1 member C3, steroid 5α reductase type 1, and AR [51]. These findings suggest that the polyphenols present in pomegranate may be useful in androgen-independent PCa and in subsets of PCa where there is up-regulation of AR. The cytochrome P450 (CYP) proteins are responsible for bioactivation of xenobiotics and endobiotics. The CYP1 isoforms activate a number of polycyclic aromatic hydrocarbons to exert their detrimental effects. Studies have shown that CYP1B1 plays an important role in the initiation and promotion of cancer and, therefore, represents an attractive target for cancer chemoprevention. It was observed that systemically available metabolites of PJ could effectively inhibit enzyme activity/expression of CYP1B1 [52]. Previous studies have shown that polymorphisms in CYP1B1 and PSA genes increased the risk of PCa [83]. Therefore, these studies suggest that consumption of PJ may reduce the incidence of PCa. A significant amount of chemopreventive studies explicitly suggest that the potential protective effect of PJ against PCa is largely attributed to ellagitanins, representing the most abundant polyphenols present in PJ. In this context, the main metabolite to concentrate in the human prostate gland upon consumption of PJ was urolithin A glucuronide, (3,8-dihydroxy-6H-dibenzo[b,d]pyran-6-one glucuronide), together with traces of urolithin B glucuronide, (3-hydroxy-6H-dibenzo[b,d]pyran-6-one glucuronide) and dimethyl ellagic acid [84]. These data indicate urolithin glucuronides and dimethyl ellagic acid may be the bioactive metabolites accounting for the chemopreventive effects of PJ against PCa.
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