ArticleFrontiers in pharmacology2020
The Curcumin Derivative, H10, Suppresses Hormone-Dependent Prostate Cancer by Inhibiting 17β-Hydroxysteroid Dehydrogenase Type 3.
Article in Frontiers in pharmacology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers, 2 of them syntheses that pooled it.
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Who cites it
8 citing papers in PubMed, 2 syntheses or guidelines pooled it.
- Curcumin in prostate cancer: a systematic review of molecular mechanisms and nanoformulated therapeutic strategies.BMC cancer · 2025Pooled it
- Application and potential value of curcumin in prostate cancer: a meta-analysis based on animal models.Frontiers in pharmacology · 2024Pooled it
- The urinary tract commensalApplied and environmental microbiology · 2026Article
- Therapeutic potentials of curcumin in prostate cancer: a comprehensive review of pathways and clinical prospects.Prostate international · 2026Review
- The Urinary Tract commensalbioRxiv : the preprint server for biology · 2026Article
- Synthesis, Anti-Tumour, and Antibacterial Activities of Monocarbonyl Curcumin Analogues of Piperidones.International journal of molecular sciences · 2025Article
- Attenuation of Scopolamine-Induced Amnesia via Cholinergic Modulation in Mice by Synthetic Curcumin Analogs.Molecules (Basel, Switzerland) · 2022Article
- Review
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10 authors.
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Abstract
The 17β-hydroxysteroid dehydrogenase type 3 (17β-HSD3) enzyme is a potential therapeutic target for hormone-dependent prostate cancer, as it is the key enzyme in the last step of testosterone (T) biosynthesis. A curcumin analog, H10, was optimized for inhibiting T production in LC540 cells that stably overexpressed 17β-HSD3 enzyme (LC540 [17β-HSD3]) (P < 0.01), without affecting progesterone (P) synthesis. H10 downregulated the production of T in the microsomal fraction of rat testes containing the 17β-HSD3 enzyme from 100 to 78.41 ± 7.41%, 51.86 ± 10.03%, and 45.14 ± 8.49% at doses of 10, 20, and 40 μM, respectively. There were no significant differences among the groups with respect to the protein expression levels of 17β-HSD3, 3βHSD1, CYP17a1, CYP11a1, and STAR, which participate in 17β-HSD3-mediated conversion of androgens to T (P > 0.05). This indicated that H10 only inhibited the enzymatic activity of 17β-HSD3
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