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

Abstract

BackgroundAccumulating 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. MethodslncRNA 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. ResultsWe 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. ConclusionOur findings provided the first evidence suggested that SOCS2-AS1 promoted the progression of glioma via upregulating ITGB1 expression.