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Knockdown of long non-coding RNA SLC8A1-AS1 attenuates cell invasion and migration in glioma via suppression of Wnt/β-catenin signaling pathways
•LncRNA SLC8A1-AS1 is up-regulated in glioma.•Knockdown of lncRNA SLC8A1-AS1 inhibited glioma cell proliferation in vitro.•LncRNA SLC8A1-AS1 regulated glioma cell invasion and migration in vitro.•Down-regulation of lncRNA SLC8A1-AS1 suppressed glioma cell Wnt/β-catenin pathway.•Silencing of lncRNA S...
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Published in: | Brain research bulletin 2021-11, Vol.176, p.112-120 |
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Main Authors: | , , , , |
Format: | Article |
Language: | English |
Subjects: | |
Citations: | Items that this one cites Items that cite this one |
Online Access: | Get full text |
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Summary: | •LncRNA SLC8A1-AS1 is up-regulated in glioma.•Knockdown of lncRNA SLC8A1-AS1 inhibited glioma cell proliferation in vitro.•LncRNA SLC8A1-AS1 regulated glioma cell invasion and migration in vitro.•Down-regulation of lncRNA SLC8A1-AS1 suppressed glioma cell Wnt/β-catenin pathway.•Silencing of lncRNA SLC8A1-AS1 repressed glioma growth in vivo.
As the most common aggressive malignant tumor in the central nervous system, glioma is still an insurmountable disease in the neural system. The mechanism of carcinogenesis in glioma remains largely unclear. In the present study, we identified a dysregulated long non-coding RNA (lncRNA) solute carrier family 8 member A1 antisense RNA 1 (SLC8A1-AS1) associated with glioma based on The Cancer Genome Atlas (TCGA) data. A validation experiment was conducted to confirm a high expression level of lncRNA SLC8A1-AS1 in glioma tissues. Down-regulation of lncRNA SLC8A1-AS1 suppressed the proliferation, colony formation, migration, and invasion of glioma cells in vitro and in vivo. Moreover, lncRNA SLC8A1-AS1 silencing decreased the activity of the Wnt/β-catenin pathway and suppressed the epithelial to mesenchymal transition (EMT) in glioma cells. These findings collectively provide novel insights into the function and mechanism of lncRNA SLC8A1-AS1 in the pathogenesis of glioma and highlight its potential as a therapeutic target for glioma intervention. |
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ISSN: | 0361-9230 1873-2747 |
DOI: | 10.1016/j.brainresbull.2021.08.011 |