LncRNA SOCS2-AS1 promotes the progression of glioma via regulating ITGB1 expression,Neuroscience Letters

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LncRNA SOCS2-AS1 promotes the progression of glioma via regulating ITGB1 expression
Neuroscience Letters ( IF 2.5 ) Pub Date : 2021-09-15 , DOI: 10.1016/j.neulet.2021.136248
Dejun Wu ₁ , Jinzhang Sun ₁ , Hongliang Wang ₁ , Chunchun Ma ₁

Affiliation

Background

Accumulating evidence has underscored the important role of long non-coding RNAs (lncRNAs) in the development and progression of glioma. However, the role of lncRNA SOCS2-AS1 in glioma is largely unknown.

Methods

lncRNA SOCS2-AS1 silencing was achieved by specific siRNAs. Proliferation of glioma cell line after lncRNA SOCS2-AS1 silencing was examined by MTT assay, Transwell assay was used to confirm changes of invasion and migration of glioma cells, and study the molecular mechanism of lncRNA SOCS2-AS1 by RT-qPCR and bioinformatics analysis.

Results

We identified that lncRNA SOCS2-AS1 was significantly upregulated in glioma, and its overexpression was closely related with malignant clinical features and poor prognosis. To explore the cellular function of SOCS2-AS1, we performed loss-of function assays in two glioma cells. We demonstrated that SOCS2-AS1 knockdown repressed glioma cell proliferation, migration and invasion. Mechanistically, SOCS2-AS1 expression was positively correlated with the expression levels of core factors ITGB1 of ECM-receptor interaction signaling pathway in glioma. Moreover, SOCS2-AS1 knockdown suppressed ITGB1 expression in glioma cells. Finally, rescue assays were carried out to determine that ITGB1 involved in SOCS2-AS1-mediated glioma cell proliferation, migration and invasion.

Conclusion

Our findings provided the first evidence suggested that SOCS2-AS1 promoted the progression of glioma via upregulating ITGB1 expression.

中文翻译：

LncRNA SOCS2-AS1通过调节ITGB1表达促进胶质瘤进展

背景

越来越多的证据强调了长链非编码 RNA (lncRNA) 在胶质瘤发展和进展中的重要作用。然而，lncRNA SOCS2-AS1 在胶质瘤中的作用在很大程度上是未知的。

方法

lncRNA SOCS2-AS1 沉默是通过特异性 siRNA 实现的。采用MTT法检测lncRNA SOCS2-AS1沉默后胶质瘤细胞系的增殖情况，Transwell法确认胶质瘤细胞侵袭迁移的变化，通过RT-qPCR和生物信息学分析研究lncRNA SOCS2-AS1的分子机制。

结果

我们发现lncRNA SOCS2-AS1在胶质瘤中显着上调，其过度表达与恶性临床特征和预后不良密切相关。为了探索 SOCS2-AS1 的细胞功能，我们在两个胶质瘤细胞中进行了功能丧失检测。我们证明了 SOCS2-AS1 敲低抑制了神经胶质瘤细胞的增殖、迁移和侵袭。机制上，SOCS2-AS1表达与胶质瘤ECM-受体相互作用信号通路核心因子ITGB1的表达水平呈正相关。此外，SOCS2-AS1 敲低抑制了胶质瘤细胞中 ITGB1 的表达。最后，进行救援试验以确定 ITGB1 参与 SOCS2-AS1 介导的胶质瘤细胞增殖、迁移和侵袭。