MiR-188-3p/GPR26 modulation functions as a potential regulator in manipulating glioma cell properties

Background: Glioblastoma (GBM) is recognized as a malignant brain tumor with frequent mortality. Extensive evidence indicated that miR-188-3p exerts an important role in various tumors. However, the role of miR-188-3p in GBM has not been elucidated. The purpose of the present investigation was to explore the biological effect of miR-188-3p, as well as to determine its target gene in GBM.Methods: The miR-188-3p and G Protein-Coupled Receptor 26 (GPR26) expressional profiles were obtained from The Cancer Genome Atlas (TCGA) database. The proliferative ability, invasive and migratory capabilities of GBM cells were measured using Cell Counting Kit-8 and transwell assays. Bioinformatics tool and luciferase reporter gene analysis were utilized to assess the correlation between miR-188-3p and GPR26. Reverse transcription-quantitative polymerase chain reaction (RT-PCR) and western blotting were performed to detect the indicated gene expression.Results: MiR-188-3p expression was highly regulated in GBM tissue and cell lines, while GPR26 was significantly decreased in GBM. Depletion of miR-188-3p significantly retarded the cell proliferation, invasion and migration in the U-87 MG cell. Luciferase reporter gene assay showed that GPR26 was a target gene of miR-188-3p in GBM. The expression of GPR26 was negatively regulated by miR-188-3p. The inhibitory effect of miR-188-3p inhibitor on cell behaviors was further strengthened by the overexpression of GPR26 in GBM.Conclusion: These findings provided evidence for the cancer-promoting effect of miR-188-3p in GBM cells and demonstrated that GPR26 was directly targeted by miR-188-3p, which might contribute to the therapeutic therapy of GBM.