Silencing of URG11 expression inhibits the proliferation and epithelial‑mesenchymal transition in benign prostatic hyperplasia cells via the RhoA/ROCK1 pathway.

Abstract

Upregulated gene 11 (URG11) represents a gene upregulated by hepatitis B virus X protein and is involved in the biological processes of multifarious tumors. The present study aimed to investigate the protective effects and regulatory mechanisms of URG11 in benign prostatic hyperplasia (BPH). URG11, Ras homolog family member A (RhoA) and Rho‑associated protein kinase 1 (ROCK1) expression was detected in patients with BPH using reverse transcription‑quantitative polymerase chain reaction (RT‑qPCR). Furthermore, URG11 expression was silenced using URG11‑targeting small interfering RNAs. In addition, cell viability was determined by performing a Cell Counting Kit‑8 assay, and the effect of URG11 on the cell cycle was investigated by flow cytometry. Expression levels of cyclin D1, p27, E‑cadherin, N‑cadherin, vimentin, RhoA and ROCK1 were investigated by RT‑qPCR and western blotting. The results revealed that the expression levels of URG11, RhoA and ROCK1 were enhanced in patients with BPH‑1 cells compared with matched healthy controls. Furthermore, it was demonstrated that transforming growth factor‑β (TGF‑β) induced the proliferation of BPH‑1 cells invitro, and silencing of URG11 inhibited the effects of TGF‑β on BPH‑1 cell proliferation and the cell cycle. In addition, silencing of URG11 altered the expression levels of cell cycle‑associated genes, epithelial‑mesenchymal transition‑associated genes, and RhoA and ROCK1 protein levels. Thus, the results of the present study suggest that URG11 may be a potential therapeutic target, which may be important to inhibit the development and progression of prostatic hyperplasia.