Modulation of AKR1C2 by curcumin decreases testosterone production in prostate cancer.
Level 5 - mechanism / opinion, no new human data
Preclinical in vitro and animal model study without human participants
PubMed 29369461 · doi:10.1111/cas.13517
What was done
Human prostate cancer cell lines (LNCaP and 22Rv1) were treated with or without curcumin, with cell proliferation measured at 0, 24, 48, and 72 hours. In vivo, transgenic adenocarcinoma of the mouse prostate (TRAMP) mice received oral curcumin at 200 mg/kg/day for 1 month. Testosterone and dihydrotestosterone concentrations in LNCaP cells were quantified using LC-MS/MS. Expression of steroidogenic acute regulatory proteins, CYP11A1, HSD3B2, and Aldo-Keto reductase 1C2 (AKR1C2) was assessed in cell lines and mouse prostate tissues.
What was found
Curcumin inhibited prostate cancer cell proliferation and induced apoptosis in a dose-dependent manner. In cell lines, curcumin decreased expression of steroidogenic acute regulatory proteins, CYP11A1, and HSD3B2, and increased AKR1C2 expression. In TRAMP mice, 1-month oral curcumin elevated prostate AKR1C2 expression and reduced tissue testosterone levels. The abstract reported no specific numerical values, percentages, or statistical significance metrics.
Why it matters
This study outlines a mechanistic pathway through which curcumin suppresses intracrine androgen synthesis and cell growth via AKR1C2 modulation in prostate cancer models.
Limits
The study is restricted to in vitro human cell lines and an animal model, precluding direct clinical translation to humans. Sample sizes for animal groups, specific in vitro concentrations, and exact numerical outcomes are not reported in the abstract. Clinical efficacy, pharmacokinetics, and safety in humans were not evaluated.
Cited by
- supports Curcumin lowers dihydrotestosterone (DHT).