LncRNA SNHG1 facilitates the epithelial-mesenchymal transition and invasiveness in glioblastoma multiforme via regulation of the miR-128-3p/RRAS2 axis

Long non-coding RNAs (lncRNAs) play an essential role in the processes of tumorigenesis and tumor development. However, the role and underlying mechanism of lncRNA small nucleolar RNA host gene 1 (SNHG1) in the development of glioblastoma multiforme (GBM) has not been fully elucidated. In this study, we found that SNHG1 was overexpressed in GBM tissue and cells. Scratch wound-healing and Transwell assays indicated that SNHG1 promoted GBM cell migration and invasion. Using bioinformatics analysis, miR-128-3p was identified as a candidate miRNA targeted by SNHG1. Dual luciferase reporter analysis indicated that miR-128-3p significantly repressed the signal from luciferase using the 3ʹ-UTR of SNHG1. Our results indicated that SNHG1 functioned as a sponge of miR-128-3p, and miR-128-3p expression was down-regulated in GBM. We also confirmed that recombinant human related RAS virus (R-Ras) oncogene homolog 2 (RRAS2) was a direct and functional target of miR-128-3p. In addition, we found that both SNHG1 and RRAS2 regulated the epithelial-mesenchymal transition (EMT) process of GBM cells. Taken together, our study showed that SNHG1 promoted the malignant progression of GBM by the SNHG1/miR-128-3p/RRAS2 axis, which activated the EMT, and which may provide a novel therapeutic treatment of GBM.