RNA binding protein immunoprecipitation (RIP) assays demonstrated that metastasis associated lung adenocarcinoma transcript 1 (MALAT1), SOX2 overlapping transcript (SOX2OT) and maternally expressed 3 (MEG3) among the 8 candidates bound to the NSPc1 protein complex in glioma H4 cells.
In summary, the present data provided novel insight into the roles of MEG3 in glioma, and MEG3/miR‑96‑5p/MTSS1 signaling could be a promising therapeutic target for the treatment of patients with glioma.
MTT assay, flow cytometry, and immunofluorescence assay were carried out to detect the impact of MEG3 on glioma cell proliferation, apoptosis, and autophagy.
In conclusion, the findings in the present study indicated that TUN treatment inhibited growth and aggressiveness through MEG-3-mediated wnt/β-catenin signaling, suggesting that TUN may be an efficient anticancer agent for the treatment of glioma.
Our study is the first to demonstrate that lncRNA MEG3 suppresses glioma cell proliferation, migration, and invasion by acting as a ceRNA of miR-19a, which provides a novel insight about the pathogenesis of glioma.
Treatment of glioma cells with the DNA methylation inhibitor 5-Aza-2'-deoxycytidine (5-AzadC) decreased aberrant hypermethylation of the MEG3 promoter and prevented the loss of MEG3 expression.