LncRNA GAS5 regulates epithelial-mesenchymal transition and viability of glioma cells by targeting microRNA-106b and regulating PTEN expression

LncRNA growth arrest special 5 (GAS5) and microRNA-106b (miR-106b) have been reported to be involved in the regulation of gliomas. However, their precise mechanisms in regulating the progression and development of gliomas remain unclear. We aimed to investigate the interaction between GAS5 and miR-106b, and their influence on the proliferation, migration, and invasion of gliomas cells. Western blotting and qRT-PCR were applied for measuring expression of protein and mRNA, respectively. The proliferation, migration, and invasion of cells were measured by MTT, wound healing, and transwell assays, respectively. Dual luciferase reporter assay was applied for confirming the binding site between miR106b and GAS5, miR-106b and PTEN. Significant higher expression of miR-106b, and lower expression of GAS5 and PTEN in the glioma tissues were observed. The binding sites between GAS5 and miR-106b, miR-106b and PTEN were identified. GAS5 could regulate the expression of PTEN through targeting miR106b, and further influence EMT process, and the proliferation, migration, and invasion of gliomas cells. Meanwhile, PTEN could remarkably inhibited the proliferation, migration and invasion of glioma cells. The influence of PTEN on glioma cells and EMT was similar to GAS5. GAS5 could regulate the EMT process, and the migration of gliomas cells through miR-106b targeting PTEN. Therefore, our findings may provide a new thought for the study of pathogenesis and treatment of glioma. (c) 2020 Elsevier B.V. and Japan Neuroscience Society. All rights reserved.

Automated summary

The study demonstrates that GAS5 and miR-106b play crucial roles in regulating the proliferation, migration, and invasion of glioma cells. GAS5 targets miR106b to influence the expression of PTEN, thereby affecting EMT process and the behavior of glioma cells. Similarly, PTEN can inhibit the proliferation, migration, and invasion of glioma cells, showing similar functions to GAS5.