Oskarsson · The Prostate 2014 · In vitro laboratory study · n=?

Inhibition of CYP17A1 activity by resveratrol, piceatannol, and synthetic resveratrol analogs.

Cited 34 times in the scientific literature.

Level 5 - mechanism / opinion, no new human data

In vitro cell culture experiment (bench research)

PubMed 24610083 · doi:10.1002/pros.22801 · record verified 2026-08-31

What was done

Human adrenocortical carcinoma cells (H295R) were treated for 24 hours with resveratrol (RSV), piceatannol (PIC), and three synthetic analogs (3,5,4'-triacetylresveratrol [RSVTA], 3,5-diacetylresveratrol [RSVDA], and 3,5,4'-trimethylresveratrol [RSVTM]) at concentrations of 1, 5, 10, 25, and 50 µM. Researchers measured steroid secretion, steroidogenic enzyme activities (notably CYP17A1 and SULT1E1), and gene expression across key steps of steroidogenesis.

What was found

All tested compounds decreased secretion of dehydroepiandrosterone (DHEA), testosterone, and cortisol at non-cytotoxic concentrations, while increasing progesterone and aldosterone secretion (no exact percentages or IC50 values were reported in the abstract). This shift was driven by inhibition of CYP17A1 enzyme activity. The synthetic analogs RSVTA, RSVDA, and RSVTM were the most efficient CYP17A1 inhibitors. RSVTM preferentially inhibited 17,20-lyase activity over hydroxylase activity. All compounds except RSVTM also increased estradiol levels, explained by inhibition of estrogen sulfoconjugation catalyzed by SULT1E1.

Why it matters

Inhibition of CYP17A1 is a key therapeutic strategy in androgen-dependent prostate cancer. Identifying that synthetic resveratrol analogs, particularly RSVTM, can selectively inhibit CYP17A1 17,20-lyase activity reveals a potential mechanistic avenue for prostate cancer chemoprevention.

Limits

This study was conducted entirely in vitro using a single human adrenocortical carcinoma cell line (H295R). In vivo pharmacokinetics, bioavailability, metabolic stability, and physiological efficacy were not assessed. The abstract reports directional shifts in steroid levels and enzyme inhibition without exact numerical values, effect sizes, or statistical variance.

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