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Bioactive tomato components inhibit cancer promoting activity of testosterone in the mouse prostate epithelium
Author(s) -
Tan Hsueh-Li,
Elsen Amy C.,
Erdman John W.,
Thomas-Ahner Jennifer M.,
Clinton Steven K.
Publication year - 2012
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.26.1_supplement.1023.4
Subject(s) - prostate cancer , castration , testosterone (patch) , prostate , androgen , endocrinology , apoptosis , medicine , carcinogenesis , chemistry , cancer , hormone , biochemistry
We hypothesize that tomato phytochemicals, such as lycopene (LYC), may antagonize cancer promoting testosterone activity in the normal prostate. C57/BL6 male mice (4 wks; n=84) consumed a control AIN93G or an identical diet with 10% tomato powder (TP) or 0.04% LYC beadlets. Mice were randomized to intact, castration, or castration + testosterone at 8 wks. Serum LYC analysis was by HPLC and prostate proliferation (Ki67) and apoptosis (ApopTag) were evaluated. Prostate gene expression was by qRT‐PCR. Serum LYC concentrations were 366 nmol/L for TP and 371 nmol/L for LYC and were reduced by castration (−38% in TP, P =0.02; −42% in LYC, P <0.001). Epithelial proliferation in TP and LYC fed intact mice was reduced by 50% ( P <0.001) with a 30% inhibition (TP, P =0.02; LYC, P <0.001) observed in the castrate‐testosterone mice. Castration dramatically enhanced apoptosis which was further increased by TP (2.2%, P <0.05). CMO1 expression is present in the liver and not detected in the prostate. The CMO2 gene, present in the liver and potentially involved in eccentric LYC cleavage, was detected in the prostate and reduced by castration ( P =0.005) with no effect of diet. Tomato phytochemicals may inhibit early prostate carcinogenesis by impacting androgen signaling pathways that impact sensitivity to early steps in the carcinogenic process. Testosterone may impact CMO2 gene expression suggesting a diet and endocrine interaction. Grant Funding Source : NIH‐NCI/AICR