MicroRNA-141 Regulates Proliferation and Apoptosis of Glioma Cells by Targeting YAP1

Glioma is one of the most common malignant tumors of the central nervous system, which is the highest incidence tumor in intracranial tumors. YAP1, the main effector factor in Hippo-YAP signaling pathway, which plays an important role in promoting cell proliferation and decreasing cell apoptosis, thus its high expression is related to the pathogenesis of glioma. The study indicates that the abnormal reduction of expression of miR-141 is associated with the pathogenesis of glioma, suggesting the possible role of the tumor suppressor. Bioinformatics analysis showed that there was a target complementary binding site between miR-141 and YAP1. The aim is to investigate whether miR-141 plays a role in regulating the expression of YAP1 and affecting the biological process of glioma cells. Tumor tissues from glioma patients were collected in this study, as well the normal traumatic brain tissue specimen were used an controls. The YAP1 expression was detected by Western blot. QRT-PCR was used to detect the expression level of miR-141 and YAP1 mRNA. Using the median of the expression levels of miR-141 and YAP1 mRNA as the boundary between high and low the survival rate of low expression and high expression of miR-141 and YAP1 mRNA was compared by Log Rank test. The target regulation between miR-141 and YAP1 was tested by the double fluoro enzyme reporter gene test. In vitro, glioma U87 and U251 cells were divided into 4 groups: miR-NC group, miR-141 mimic group, siRNA-NC group and si-YAP1 group. QRT-PCR and Western blot were used to detect the expression of YAP1, apoptosis was detected by flow cytometry, and cell proliferation was detected by means of EdU staining. In this study, the decrease of miR-141 expression and the increase of YAP1 expression were related to the pathogenesis of glioma, and its expression were related to the survival rate. MiR-141 could inhibit the expression of YAP1, obviously weakened the proliferation of glioma cells and induced apoptosis.