ArticleMolecular biomedicine2024
Y-27632 targeting ROCK1&2 modulates cell growth, fibrosis and epithelial-mesenchymal transition in hyperplastic prostate by inhibiting β-catenin pathway.
Article in Molecular biomedicine, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed.
- Inhibition of 5αR2 promotes postoperative wound repair in BPH patients after TURP by alleviating fibrosis and inflammation.Asian journal of andrology · 2026Trial
- The effects of netarsudil ophthalmic solution on the expression of genes involved in fibrogenesis in orbital fibroblasts of patients with thyroid eye disease.Molecular biology reports · 2026Article
- Global stagnation and misaligned priorities in BPH drug development: a 25-year landscape analysis of clinical trial registries.npj aging · 2026Article
- Rho-related GTP-binding protein RhoE (RND3) regulates multiple myeloma bone disease.Cancer cell international · 2026Article
- Fibroblasts promote the progression of benign prostatic hyperplasia through colony-stimulating factor 1 receptor-mediated RTK signaling in prostatic epithelial cells.Molecular biomedicine · 2025Article
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13 authors.
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Abstract
Benign prostatic hyperplasia (BPH) is a prevalent condition affecting the male urinary system, with its molecular mechanisms of pathogenesis remaining unclear. Y-27632, a non-isoform-selective Rho kinase inhibitor, has shown therapeutic potential in various diseases but its effects on static factors and fibrosis in BPH remain unexplored. This study investigated human prostate tissues, human prostate cell lines, and BPH rat model using immunofluorescence, flow cytometry, quantitative reverse transcription polymerase chain reaction, western blotting, and cell counting kit-8. ROCK1 and ROCK2 were significantly up-regulated in BPH tissues, correlating with clinical parameters. Y-27632 targeted the inhibition of ROCK1 & ROCK2 expression and inhibited cell proliferation, fibrosis, epithelial-mesenchymal transition (EMT), while induced cell apoptosis in a dose-dependent manner. Moreover, knockdown of either ROCK isoform inhibited fibrosis and EMT, induced apoptosis, while ROCK overexpression had the opposite effects. ROCK downregulation inhibited the β-catenin signaling pathway (such as C-MYC, Snail and Survivin) and decreased β-catenin protein stability, while inhibiting TGF-β/Smad
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