High glucose induces the proliferation of prostatic cells via downregulating MRE11.

The aim of the present study was to investigate the candidate genes and pathways associated with benign prostatic hyperplasia (BPH) and diabetes. In vitro experiments were performed using normal prostatic epithelial RWPE‑1 and HPr‑1 cells. The cell lines were treated with a high‑glucose solution and MTS and bromodeoxyuridine assays were used to assess cell viability. Transcriptome sequencing was used to screen the candidate genes. The expression of candidate genes was further verified by reverse transcription‑quantitative polymerase chain reaction (RT‑qPCR) and western blotting. A meiotic recombination 11 (MRE11) overexpression vector was designed and transfected into RWPE‑1 cells to verify the function of MRE11. A streptozotocin‑induced diabetic rat model was established and rat MRE11 levels were determined by RT‑qPCR and immunohistochemical staining. High concentrations of glucose resulted in RWPE‑1 and HPr‑1 cells with high viability. Transcriptome sequencing revealed that MRE11 was downregulated when RWPE‑1 cells were exposed to high‑glucose conditions. When MRE11 was overexpressed, cell viability decreased and cell apoptosis was induced under high‑glucose conditions. Prostatic tissues from rats were collected and assessed; MRE11 expression was observed to be decreased, which was consistent with the in vitro cell experiments. BPH may be associated with diabetes, as MRE11 expression in prostatic cells was decreased when exposed to high‑glucose conditions. Therefore, MRE11 may have potential as a biomarker for the early diagnosis of BPH and diabetes.