Resveratrol suppresses prostate cancer progression in transgenic mice.
Level 5 - mechanism / opinion, no new human data
Bench and animal research (transgenic mouse model) without human clinical data
PubMed 17675339 · doi:10.1093/carcin/bgm144
What was done
Transgenic Adenocarcinoma Mouse Prostate (TRAMP) male mice were fed either a diet containing resveratrol (625 mg/kg AIN-76A diet) or a phytoestrogen-free control diet (AIN-76A) starting at 5 weeks of age. Signaling mechanisms were evaluated at 12 weeks of age and histopathology was assessed at 28 weeks of age. Serum sex steroids, sex hormone-binding globulin (SHBG), prostatic SV40 large T antigen expression, and serum resveratrol levels were also measured.
What was found
Dietary resveratrol significantly reduced the incidence of poorly differentiated prostatic adenocarcinoma by 7.7-fold. In the dorsolateral prostate, resveratrol significantly inhibited cell proliferation, decreased IGF-1 and phospho-ERK 1, and increased androgen receptor, estrogen receptor-beta, and IGF-1 receptor. In the ventral prostate, it significantly reduced cell proliferation and phospho-ERKs 1 and 2, but did not significantly alter IGF-1 or IGF-1 receptor. Serum levels of total testosterone, free testosterone, estradiol, dihydrotestosterone, SHBG, and SV40 large T antigen expression were unchanged. Total serum resveratrol at 12 weeks was 52 +/- 18 nM.
Why it matters
This study provides mechanistic evidence in a transgenic mouse model that oral resveratrol inhibits prostate cancer progression and down-regulates proliferative growth signaling locally without disrupting systemic circulating sex hormone concentrations.
Limits
This is an animal study using transgenic mice; findings cannot be directly applied to human prostate cancer prevention. Total sample size (n), variance data for tumor incidence reduction, and dose-response dynamics were not reported in the abstract.
Cited by
- partial Megadoses of resveratrol decrease androgen levels in prostate cancer models.