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

• Published in: Neuroscience letters Vol. 765; p. 136248
• Main Authors: Wu, Dejun, Sun, Jinzhang, Wang, Hongliang, Ma, Chunchun
• Format: Journal Article
• Language: English
• Published: Ireland Elsevier B.V 20-11-2021
• Subjects: Astrocytes; Brain - pathology; Brain Neoplasms - diagnosis; Brain Neoplasms - genetics; Brain Neoplasms - mortality; Brain Neoplasms - pathology; Cell Line, Tumor; Cell Movement - genetics; Cell Proliferation - genetics; Computational Biology; Datasets as Topic; Gene Expression Regulation, Neoplastic; Gene Knockdown Techniques; Glioma; Glioma - diagnosis; Glioma - genetics; Glioma - mortality; Glioma - pathology; Humans; Integrin beta1 - genetics; ITGB1; lncRNAs; Neoplasm Grading; Neoplasm Invasiveness - genetics; Prognosis; RNA, Long Noncoding - genetics; RNA, Long Noncoding - metabolism; SOCS2-AS1; Survival Rate; Up-Regulation; lncRNAs; ITGB1; Glioma; SOCS2-AS1
• ISSN: 0304-3940; 1872-7972
• DOI: 10.1016/j.neulet.2021.136248

•The upregulation of SOCS2-AS1 is associated with prognosis in gliomas.•Knockdown of SOCS2-AS1 inhibits the growth of glioma cell.•SOCS2-AS1 is associated with ECM-receptor interaction signaling pathway.•SOCS2-AS1 regulate ITGB1 express in glioma.•ITGB1 mediates the tumor-suppressive effects of SOCS2-AS1 knockdown.
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.