ArticleiScience2024
YAP-mediated GPER signaling impedes proliferation and survival of prostate epithelium in benign prostatic hyperplasia.
Article in iScience, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 10 citations in OpenAlex.
- Association between the G-protein-coupled estrogen receptor 1 and prostate cancer in the Slovak population.Molecular biology reports · 2026Article
- miR-16-5p mediates E2-induced cell proliferation and EMT in benign prostate hyperplasia.Scientific reports · 2026Article
- Targeting ROCK1/YAP1 Axis Ameliorates Inflammation-Induced Prostatic Hyperplasia via Stabilising SIRT1-Dependent Mitochondrial Dynamics.Cell proliferation · 2026Article
- Decoding benign prostatic hyperplasia at single-cell resolution: heterogeneity, inflammation, and beyond androgen-driven pathogenesis.Frontiers in immunology · 2026Review
- The role of phosphatidylinositol (18:1_18:1) in benign prostatic hyperplasia: an integrated study of Mendelian randomization and network pharmacology.World journal of urology · 2025Article
- Tracing the Evolution of Sex Hormones and Receptor-Mediated Immune Microenvironmental Differences in Prostate and Bladder Cancers: From Embryonic Development to Disease.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Review
- Network pharmacology and experimental validation to explore the pharmacological mechanism of saw palmetto and its core ingredients in benign prostatic hyperplasia treatment.Naunyn-Schmiedeberg's archives of pharmacology · 2025Article
- The pathogenesis of benign prostatic hyperplasia and the roles of Prdx3, oxidative stress, pyroptosis and autophagy:a review.Frontiers in oncology · 2025Review
- Therapeutic Effect of Brain Awakening and Mind Opening Acupuncture Combined with Simiao Pill on Mice with Benign Prostatic Hyperplasia.Journal of inflammation research · 2025Article
- The miRNAs 203a/210-3p/5001-5p regulate the androgen/androgen receptor/YAP-induced migration in prostate cancer cells.Cancer medicine · 2024Article
Corrections and comments
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Authors and funding
12 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Benign prostatic hyperplasia (BPH) occurs when there is an imbalance between the proliferation and death of prostate cells, which is regulated tightly by estrogen signaling. However, the role of G protein-coupled estrogen receptor (GPER) in prostate cell survival remains ambiguous. In this study, we observed that prostates with epithelial hyperplasia showed increased yes-associated protein 1 (YAP) expression and decreased levels of estrogen and GPER. Blocking YAP through genetic or drug interventions led to reduced proliferation and increased apoptosis in the prostate epithelial cells. Interestingly, GPER agonists produced similar effects. GPER activation enhanced the phosphorylation and degradation of YAP, which was crucial for suppressing cell proliferation and survival. The Gαs/cAMP/PKA/LATS pathway, downstream of GPER, transmitted signals that facilitated YAP inhibition. This study investigated the interaction between GPER and YAP in the prostate epithelial cells and its contribution to BPH development. It lays the groundwork for future research on developing BPH treatments.
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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.