Background
LncRNA GAS8-AS1 has been reported to participate in several types of cancer, while its role in glioblastoma (GBM) is unknown. In the present study, we aimed to investigate the function of GAS8-AS1 in GBM and the underlying mechanisms.
Conclusion
Overexpression of GAS8-AS1 inhibits GBM cell proliferation and invasion by downregulating NEAT1.
Methods
The expression levels of GAS8-AS1 and NEAT1 in GBM patients and the healthy controls were measured by performing RT-qPCR. Diagnostic values of plasma GAS8-AS1 and NEAT1 for GBM were analyzed by performing ROC curve analysis with GBM patients as true positive cases and the healthy controls as true negative cases. Linear regression analysis was performed to study the correlation between the expression levels of GAS8-AS1 and NEAT1. The expression levels of GAS8-AS1 and NEAT1 in GBM cells were also determined by RT-qPCR. CCK-8 and transwell invasion assays were performed to detect the proliferation and invasion of GBM cells. Western blot assay was performed to detect the expression levels of β-catenin, Axin2, c-myc, cyclin D1, and GAPDH in GBM cells.
Results
GAS8-AS1 was downregulated, while lncRNA NEAT1 was upregulated in the plasma of GBM patients. Altered expression levels of GAS8-AS1 and NEAT1 distinguished GBM patients from the healthy controls. The expression of GAS8-AS1 and NEAT1 was inversely correlated only in GBM patients. Overexpression of GAS8-AS1 reduced the expression levels of NEAT1 in GBM cells, while knock-down of GAS8-AS1 increased the expression levels of NEAT1. However, overexpression of NEAT1 showed no significant effects on the expression of GAS8-AS1. Knock-down of GAS8-AS1 promoted GBM cell proliferation and invasion and enhanced the activation of the Wnt/β-catenin pathway. However, the effects of knock-down of GAS8-AS1 were alleviated by the knock-down of NEAT1.