Study on the roles of glycolipid metabolism indicators and microRNAs in benign prostatic hyperplasia

Abstract Objectives As a highly prevalent disease in older men, the incidence of benign prostatic hyperplasia (BPH) is increasing as aggravating aging of the global population. This study aimed to explore the pathogenesis of BPH and its potential biomarkers. Methods Expression of miR-96-5p/miR-181a-5p and glycolipid metabolism indicators (GLMI) were detected by collecting the peripheral blood samples from 100 healthy volunteers and 110 patients with BPH. The diagnostic value of clinical factors for BPH was evaluated through the receiver operating characteristic (ROC) curve. The inhibitors of miR-96-5p and miR-181a-5p were introduced to detect their roles in BPH pathogenesis and regulation of FOXP2 expression. Interaction between miR-96-5p/miR-181a-5p and FOXP2 mRNA was verified through dual luciferase assay. Silencing FOXP2 to explore its role in the progression of BPH. Results GLMI, miR-96-5p, and miR-181a-5p levels are high in BPH patients and increased with the severity of disease, and their blood levels are positively correlated with International Prostate Symptom Score (IPSS). MiR-96-5p combined with miR-181a-5p is a good prediction model for the occurrence and severe progression of BPH, with area under curve (AUC) of 0.901 and 0.927, respectively; and they combined with GLMI showed a high authenticity, with AUC of 0.927 and 0.962, respectively. MiR-96-5p/miR-181a-5p inhibited FOXP2 expression by adsorption of its mRNA, and their inhibition reduced the viability and promoted apoptosis of WPMY-1 and BPH-1 cells, which was reversed by the silence of FOXP2. Conclusions GLMI, miR-96-5p, and miR-181a-5p presented a close clinical correlation with BPH, which are valuable biomarkers of BPH, and these two miRNAs may contribute to BPH progression by regulating FOXP2 negatively.