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

胶质瘤 SOCS2 癌症研究 生物 抑制器 癌症 遗传学
作者
Dejun Wu,Jinzhang Sun,Hongliang Wang,Chunchun Ma
出处
期刊:Neuroscience Letters [Elsevier]
卷期号:765: 136248-136248 被引量:9
标识
DOI:10.1016/j.neulet.2021.136248
摘要

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