Long non-coding RNA SNHG11 promotes cell proliferation, invasion and migration in glioma by targeting miR-154-5p.

Abstract

Long non-coding RNAs (lncRNAs) play critical roles in tumour progression. However, the function of lncRNA small nucleolar RNA host gene 11 (SNHG11) in glioma has not been mentioned before. Our study aims to uncover the biological roles of SNHG11 in the progression of glioma and throw light for clinical treatment of glioma. The Gene Expression Profiling Interactive Analysis (GEPIA) dataset was used to analyze the SNHG11 expression between glioma and normal tissue, as well as survival benefit. The quantitative Real Time-Polymerase Chain Reaction (qRT-PCR) was used to detect SNHG11 and miR-154-5p expression. Celltiter-Glo, colony formation, and transwell assays were utilized to detect the influence of SNHG11 to the malignancy of U87 and U251 cells. The underlying pathways affected by SNHG11 were measured using Western blot. Furthermore, Luciferase reporter assay was applied to verify the interaction between SNHG11 and miR-154-5p. SNHG11 was upregulated in glioblastoma tissues and five malignant glioma cell lines. SNHG11 expression was negatively correlated with overall survival of glioma patients. Moreover, silencing of SNHG11 could decrease glioma cell viability both in vitro and in vivo. Furthermore, the inhibition of SNHG11 suppressed proliferation, invasion and migration via regulating epithelial-mesenchymal transition (EMT). In addition, SNHG11 could bind miRNA-154-5p and negatively regulate its level. SNHG11 functioned as an oncogene in glioma and promoted proliferation, invasion, and migration via EMT by sponging miR-154-5p. These findings provided a new therapeutic target for glioma.