Document Type
Article
Version Deposited
Published Version
Publication Date
10-26-2024
Publication Title
Molecular Biomedicine
DOI
10.1186/s43556-024-00216-9
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
Recommended Citation
Shan, S., Su, M., Wang, H. et al. Y-27632 targeting ROCK1&2 modulates cell growth, fibrosis and epithelial-mesenchymal transition in hyperplastic prostate by inhibiting β-catenin pathway. Mol Biomed 5, 52 (2024). https://doi.org/10.1186/s43556-024-00216-9
Creative Commons License
This work is licensed under a Creative Commons Attribution 4.0 International License.
Comments
Open Access This article is licensed under a Creative Commons Attribution 4.0 International License.
Molecular Biomedicine is an Open Access journal published by Springer Nature.