ArticleThe Journal of pathology2017
Androgenic to oestrogenic switch in the human adult prostate gland is regulated by epigenetic silencing of steroid 5α-reductase 2.
Article in The Journal of pathology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
25 citing papers in PubMed, 38 citations in OpenAlex.
- Trial
- SRD5A2 and emerging therapies in androgen-driven disorders.Nature reviews. Urology · 2026Review
- A single cell transcriptional profile of benign prostatic hyperplasia.Scientific reports · 2026Article
- Estrogen regulation in the prostate underlies racial disparity in men with benign prostatic hyperplasia.The Journal of pathology · 2026Article
- Nanomedicine for Benign Prostatic Hyperplasia: Pathological Axes and Translational Evidence.International journal of nanomedicine · 2026Review
- Stromal Steroid 5 Alpha-Reductase 2 Promotes Prostate Growth through WNT5A-Lymphoid Enhancer-Binding Factor 1-Insulin-Like Growth Factor 1 Signaling in Benign Prostatic Hyperplasia.The American journal of pathology · 2025Article
- Unveiling therapeutic targets and preventive components for kidney insufficiency and blood stasis-type BPH: bridging metabolomics, network pharmacology and reverse screening.Frontiers in pharmacology · 2025Article
- Ectonucleotidases and purinergic receptors in mouse prostate gland.American journal of clinical and experimental urology · 2025Article
- Zhuangyao Jianshen pill ameliorates testosterone-induced benign postatic hyperplasia in rats.Journal of traditional Chinese medicine = Chung i tsa chih ying wen pan · 2024Article
- Enhanced prostatic Esr1The Journal of pathology · 2024Article
- Intrinsic and extrinsic factors causing hyperplasia of the prostate.International journal of urology : official journal of the Japanese Urological Association · 2024Review
- Effects of Taraxaci Herba (Dandelion) on Testosterone Propionate-Induced Benign Prostatic Hyperplasia in Rats.Nutrients · 2024Article
- Sex steroid hormone residues in milk and their potential risks for breast and prostate cancer.Frontiers in nutrition · 2024Review
- Exploring the Enigma of 5-ARIs Resistance in Benign Prostatic Hyperplasia: Paving the Path for Personalized Medicine.Current urology reports · 2023Review
- Upregulation of mir-1199-5p is associated with reduced type 2 5-α reductase expression in benign prostatic hyperplasia.BMC urology · 2022Article
- Estrogen and G protein-coupled estrogen receptor accelerate the progression of benign prostatic hyperplasia by inducing prostatic fibrosis.Cell death & disease · 2022Article
- Intra-epithelial non-canonical Activin A signaling safeguards prostate progenitor quiescence.EMBO reports · 2022Article
- Article
- Proteinarium: Multi-sample protein-protein interaction analysis and visualization tool.Genomics · 2020Article
- Obesity-associated inflammation induces androgenic to estrogenic switch in the prostate gland.Prostate cancer and prostatic diseases · 2020Observational
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
12 authors at 3 institutions in 2 countries.
Funding
Abstract
Benign prostatic hyperplasia is the most common proliferative abnormality of the prostate. All men experience some prostatic growth as they age, but the rate of growth varies among individuals. Steroid 5α-reductase 2 (SRD5A2) is a critical enzyme for prostatic development and growth. Previous work indicates that one-third of adult prostatic samples do not express SRD5A2, secondary to epigenetic modifications. Here we show that the level of oestradiol is dramatically elevated, concomitant with significant upregulation of oestrogen response genes, in prostatic samples with methylation at the SRD5A2 promoter. The phosphorylation of oestrogen receptor-α in prostatic stroma is upregulated when SRD5A2 expression is absent. We show that tumour necrosis factor (TNF)-α suppresses SRD5A2 mRNA and protein expression, and simultaneously promotes expression of aromatase, the enzyme responsible for conversion of testosterone to oestradiol. Concomitant suppression of SRD5A2 and treatment with TNF-α synergistically upregulate the aromatase levels. The data suggest that, in the absence of prostatic SRD5A2, there is an androgenic to oestrogenic switch. These findings have broad implications for choosing appropriate classes of medications for the management of benign and malignant prostatic diseases. Copyright © 2017 Pathological Society of Great Britain and Ireland. Published by John Wiley & Sons, Ltd.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.