Abstract
Background: Long non-coding RNAs (lncRNAs) are increasingly being regarded as regulators of glioma development. Notably, some studies report that GNG12-AS1 plays important functions and molecular mechanism in breast cancer, but there are no existing studies in glioma.Objective: To analyze the biological functions and potential mechanisms of GNG12-AS1 in glioma.Methods: We detected the expression of GNG12-AS1 in glioma tissues through analyzing TCGA data as well as our clinical samples. We then evaluated cell proliferation through MTT assay and colony formation and cell migration by transwell assay, wound healing assay and single cell tracking assay. After, we analyzed the effects of the AKT/GSK-3β/β-catenin through Western blotting and utilized the β-catenin agonist SKL2001 for the rescue experiment.Results: GNG12-AS1 was highly expressed in glioma tissues. The silence of GNG12-AS1 inhibited the proliferation, migration and epithelial–mesenchymal transition of glioma cells, and reduced the activity of the AKT/GSK-3β/β-catenin pathway. Notably, SKL2001 could reverse cell migration as well as β-catenin expression in glioma cells with lower GNG12-AS1 expression.Conclusions: GNG12-AS1 regulates proliferation and migration of glioma cells through the AKT/GSK-3β/β-catenin signaling and can perhaps be a new target for the treatment of glioma.
Highlights
Glioma is one of the most common primary brain tumors in adults and has a 5-year survival rate of approximately 5% [1]
Previous studies have indicated that a novel Long non-coding RNAs (lncRNAs), lnc GNG12-AS1, is highly expressed in the pancreas, small intestine, testes, liver, breasts, cervix and adipose tissue
We discovered that the expression of GNG12-AS1 was higher in glioma tissues than in normal tissues
Summary
Glioma is one of the most common primary brain tumors in adults and has a 5-year survival rate of approximately 5% [1]. Glioma can undergo highly invasive growth, which makes the tumor extremely prone to recurrence [3]. Based on such factors, it is necessary to identify the molecular mechanisms of glioma occurrence and development, and to discover specific biomarkers and therapeutic targets for glioma. There is mounting evidence that lncRNA genes are similar to protein coding genes in some key respects, and they have realized important molecular functions in many cellular pathways and processes [5]. The silence of GNG12-AS1 inhibited the proliferation, migration and epithelial–mesenchymal transition of glioma cells, and reduced the activity of the AKT/GSK-3β/β-catenin pathway. Conclusions: GNG12-AS1 regulates proliferation and migration of glioma cells through the AKT/GSK-3β/β-catenin signaling and can perhaps be a new target for the treatment of glioma
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