LncRNA SNHG7 promotes glioma cells viability, migration and invasion by regulating miR-342-3p/AKT2 axis.

Glioma has been categorized as the most common primary malignant brain tumor. Long non-coding RNA SNHG7 (lncRNA SNHG7) has been recognized in various cancers as a possible oncogene. In this study, the effect of SNHG7 on glioma cells was investigated. Thirty glioma tissues and adjacent normal tissues were collected. Pc-SNHG7, sh-SNHG7, miR-342-3p mimic and miR-342-3p inhibitor were transfected into the glioma cells. Cell Counting Kit-8, Transwell and scratch assay evaluated glioma cells viability, invasion and migration, respectively. TargetScan, Starbase and dual-luciferase reporter were used to predict and confirm the target genes and potential binding sites of SNHG7, miR-342-3p and AKT2. Relative miR-342-3p and AKT2 expressions were assessed by quantitative real-time polymerase chain reaction (qRT-PCR) and western blot. Pearson's analysis was adopted for correlation analysis between SNHG7, miR-342-3p and AKT2. SNHG7 expressions in glioma tissues and cells were increased, upregulation of SNHG7 promotes cell viability, invasion and migration. SNHG7 was shown to bind with miR-342-3p, and upregulating SNHG7 reduced miR-342-3p expression. AKT2 was the target gene of miR-342-3p, and miR-342-3p expression was decreased while AKT2 expression was increased in glioma tissues. High expression of miR-342-3p inhibited cell viability, invasion and migration and reduced AKT2 expression, whereas low expression of miR-342-3p did the opposite effect. Upregulating SNHG7 might promote glioma cells viability, migration and invasion with the regulation of decreasing miR-342-3p level and increasing AKT2 level. [ABSTRACT FROM AUTHOR]