Cheng Gaopeng, Zheng Jian, Wang Long
Department of Neurosurgery, Heping Hospital Affiliated to Changzhi Medical College, Changzhi City, China.
Department of Electro Cardiogram, Shanxi Provincial Cancer Hospital, China.
Int J Neurosci. 2021 Dec;131(12):1190-1202. doi: 10.1080/00207454.2020.1790556. Epub 2020 Sep 29.
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.
胶质瘤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）在多种癌症中被认为是一种可能的癌基因。在本研究中，研究了SNHG7对胶质瘤细胞的影响。
收集30例胶质瘤组织及相邻正常组织。将Pc-SNHG7、sh-SNHG7、miR-342-3p模拟物和miR-342-3p抑制剂转染到胶质瘤细胞中。细胞计数试剂盒-8、Transwell实验和划痕实验分别评估胶质瘤细胞的活力、侵袭和迁移能力。使用TargetScan、Starbase和双荧光素酶报告基因预测并确认SNHG7、miR-342-3p和AKT2的靶基因及潜在结合位点。通过定量实时聚合酶链反应（qRT-PCR）和蛋白质免疫印迹法评估miR-342-3p和AKT2的相对表达。采用Pearson分析对SNHG7、miR-342-3p和AKT2之间进行相关性分析。
胶质瘤组织和细胞中SNHG7表达增加，SNHG7上调促进细胞活力、侵袭和迁移。SNHG7与miR-342-3p结合，上调SNHG7会降低miR-342-3p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高表达抑制细胞活力、侵袭和迁移并降低AKT2表达，而miR-342-3p低表达则产生相反作用。
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。
