LINC01207 Predicts Poor Prognosis and Suppresses Cell Growth and Metastasis via Regulating GSK-3β/β-Catenin Signaling Pathway in Malignant Glioma.

Abstract

BackgroundRecent literature has revealed that LINC01207 plays a vital part in tumorigenesis and malignancy progression. However, the potential mechanisms of LINC01207 in malignant glioma are still unknown.Material/MethodsQuantitative real-time polymerase chain reaction (qRT-PCR) was applied to analyze LINC01207 mRNA levels in malignant glioma cell lines and tissue samples. The correlation between LINC01207 mRNA levels and clinical characteristics was explored, and the relative survival rate was observed using the Kaplan-Meier method. To examine the function of LINC01207, we performed cell viability, EdU assay, cell cycle assay, Transwell assay, and wound-healing assay to analyze relative cell proliferation, migration/invasion ability. Finally, qRT-PCR and western blot were used to investigate the potential mechanisms.ResultsLINC01207 mRNA was lowly expressed in malignant glioma cells and cancer tissue samples. Low expression of LINC01207 was associated with Karnofsky performance score (KPS), invasion condition, and tumor grade. Moreover, multivariate analysis confirmed LINC01207 expression and tumor grade were significant independent predictors of poor survival in malignant glioma. LINC01207 markedly inhibited cellar proliferation and viability via inducing G0/G1 phase cell cycle arrested and repressed cell metastasis through restraining epithelial-to-mesenchymal procession in vivo. In addition, we detected a reduction in the protein levels of β-catenin and p-GSK-3β, while GSK-3β expression was upregulated.ConclusionsIn summary, LINC01207 served as a tumor-related tumor suppress gene for malignant glioma through inhibiting of GSK-3β/β-catenin signaling pathway.