MicroRNA218 inhibits glioma migration and invasion via inhibiting glioma-associated oncogene homolog 1 expression at N terminus

Glioma is characterized by high invasion, migration and proliferation abilities. However, the molecular mechanism that triggers the development and recurrence of this tumor is also elusive. This study aims to investigate the biological function and molecular mechanism of microRNA218 in glioma. Human glioma samples were obtained and employed to investigate the correlation between microRNA218 and glioma pathological grading. Glioma cell viability was detected by the cell-counting kit-8 (CCK-8) cell counting assay. Transwell assay and wound-healing assay were employed to examine the migration and invasion of the glioma cells. The mRNA transcription and protein expression of glioma-associated oncogene homolog 1 (GLI1) were analyzed by quantitative RT-PCR and Western blot analysis, respectively. Southwestern blot assay was utilized to explore the possible interaction site of GLI1 and microRNA218. The results indicated that microRNA218 is significantly down-regulated in glioma samples and negatively correlated with the pathological grading. The cell viability was significantly decreased, and migration and invasion were significantly inhibited in microRNA218 treated cells, compared with un-treated cells. GLI1 was discovered acting as a functional downstream target of microRNA218, by which microRNA218 inhibited glioma cell migration and invasion. Southwestern blot result showed that microRNA218 targeted directly the N terminus of GLI1 molecular, and repressed the GLI1 expression in U87MG cells. In conclusion, microRNA218 could reduce the invasion and migration, and inhibit proliferation of glioma cells by suppressing the expression of GLI1 protein at the interacting with the N terminus.