Knockdown of long non-coding RNA SLC8A1-AS1 attenuates cell invasion and migration in glioma via suppression of Wnt/β-catenin signaling pathways

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. Downregulation 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/ fi-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.

Automated summary

Glioma, the most common aggressive malignant tumor in the central nervous system, has unclear mechanisms of carcinogenesis. The dysregulated lncRNA SLC8A1-AS1 was found to be highly expressed in glioma and its downregulation inhibited tumor cell proliferation, migration, and invasion, as well as suppressed the Wnt/β-catenin pathway and epithelial to mesenchymal transition. This suggests the potential of lncRNA SLC8A1-AS1 as a therapeutic target for glioma intervention.