Lnc GNG12-AS1 knockdown suppresses glioma progression through the AKT/GSK-3β/β-catenin pathway.

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.