Microrna-137 Regulates Hypoxia-Mediated Migration And Epithelial-Mesenchymal Transition In Prostate Cancer By Targeting Lgr4 Via The Egfr/Erk Signaling Pathway

MicroRNAs (miRs) serve an integral role in prostate cancer. The present study aimed to investigate the effects and mechanisms of miR-137 in hypoxia-mediated migration and epithelial-mesenchymal transition (EMT). PC3 and DU145 prostate cancer cells were exposed to hypoxia for 24 h, after which the expression of miR-137 was determined by reverse transcription-quantitative PCR (RT-qPCR). The cells were transfected with a miR-137 mimic or inhibitor, followed by hypoxia exposure. The results demonstrated that hypoxia reduced miR-137 expression. Further results from the Cell Counting Kit-8, Cell Death Detection ELISA plus kit, Transwell assay, RT-qPCR and western blotting assays revealed that the miR-137 mimic prevented cell proliferation, facilitated apoptosis and repressed cell migration, invasiveness, and expression of N-cadherin, vimentin and matrix metalloproteinase 2; the miR-137 inhibitor exerted the opposite effects. A dual-luciferase reporter assay determined that miR-137 directly targeted leucine-rich repeat-containing G protein-coupled receptor 4 (LGR4). Additionally, miR-137 negatively regulated the epidermal growth factor receptor/extracellular signal-regulated kinase (EGFR/ERK) signaling pathway by targeting LGR4. LGR4 silencing or EGFR/ERK inhibition abolished the effects of miR-137 inhibitor on cell migration and EMT. In conclusion, by targeting LGR4 via the EGFR/ERK signaling pathway, miR-137 inhibited prostate cancer cell migration and EMT.