Liu D, Liu J, Li Y, et al. - According to novel findings in this study, cell proliferation and the epithelial–mesenchymal transition (EMT) process in benign prostatic hyperplasia (BPH) are modulated by bone morphogenetic protein 5 (BMP5) via the BMP/Smad signaling pathway which could contribute to the development of BPH. BMP/Smad signaling may be re-identified as a promising new treatment target for BPH management.

• According to recent studies, BMP5 is upregulated in BPH tissues.

• Human prostate cell lines (BPH-1, WPMY-1) and human/rat hyperplastic prostate tissues were used.

• Upregulation of BMP5 was found in human and rat hyperplastic tissues, and BMP5 was localized both in the epithelial and stromal compartments of the prostate tissues.

• Cell proliferation and the EMT process were enhanced by BMP5 overexpression through phosphorylation of Smad1/5/8, while BMP5 knockdown caused cell cycle arrest at G0/G1 phase and blocked the EMT process.

• The impacts of BMP5 silencing and overexpression were reversed by a BMP/Smad signaling pathway agonist and antagonist, respectively.

• In addition, a positive correlation of BMP5 expression with prostate volume as well as with total prostate-specific antigen was evident.