Abstract

Purpose

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.

Materials and methods

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.

Results

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.

Conclusions

Upregulating SNHG7 might promote glioma cells viability, migration and invasion with the regulation of decreasing miR-342-3p level and increasing AKT2 level.

中文翻译：

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LncRNA SNHG7 通过调节 miR-342-3p/AKT2 轴促进胶质瘤细胞的活力、迁移和侵袭

摘要

目的

胶质瘤已被归类为最常见的原发性恶性脑肿瘤。长链非编码 RNA SNHG7 (lncRNA SNHG7) 已在各种癌症中被认为是一种可能的致癌基因。在这项研究中，研究了 SNHG7 对胶质瘤细胞的影响。

材料和方法

收集了三十个神经胶质瘤组织和邻近的正常组织。将 Pc-SNHG7、sh-SNHG7、miR-342-3p mimic 和 miR-342-3p inhibitor 转染到胶质瘤细胞中。Cell Counting Kit-8、Transwell 和划痕试验分别评估了胶质瘤细胞的活力、侵袭和迁移。TargetScan、Starbase 和双荧光素酶报告基因用于预测和确认 SNHG7、miR-342-3p 和 AKT2 的靶基因和潜在结合位点。通过定量实时聚合酶链反应（qRT-PCR）和蛋白质印迹评估相对 miR-342-3p 和 AKT2 表达。SNHG7、miR-342-3p和AKT2之间的相关性分析采用Pearson分析。

结果

SNHG7在胶质瘤组织和细胞中的表达增加，上调SNHG7促进细胞活力、侵袭和迁移。SNHG7 与 miR-342-3p 结合，上调 SNHG7 可降低 miR-342-3p 的表达。AKT2是miR-342-3p的靶基因，在胶质瘤组织中miR-342-3p表达降低而AKT2表达增加。miR-342-3p 的高表达抑制细胞活力、侵袭和迁移并降低 AKT2 的表达，而 miR-342-3p 的低表达则产生相反的效果。

结论

上调 SNHG7 可能通过降低 miR-342-3p 水平和增加 AKT2 水平来促进胶质瘤细胞的活力、迁移和侵袭。