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

BACKGROUND Recent 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 AND METHODS Quantitative 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. RESULTS LINC01207 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 ß-catenin and p-GSK-3ß, while GSK-3ß expression was upregulated. CONCLUSIONS In summary, LINC01207 served as a tumor-related tumor suppress gene for malignant glioma through inhibiting of GSK-3ß/ß-catenin signaling pathway.

Spalt-Like Transcription Factor 1 (SALL1) Gene Expression Inhibits Cell Proliferation and Cell Migration of Human Glioma Cells Through the Wnt/ß-Catenin Signaling Pathway.

BACKGROUND The spalt-like transcription factor 1 (SALL1) gene is a member of the Krüppel-associated box-containing zinc finger proteins (KRAB-ZFPs) and has been shown to modulate the onset and progression of human tumors. This study aimed to investigate the regulatory effects and mechanisms of SALL1 gene expression in human glioblastoma and glioma cells and tissue samples from patients with cerebral glioma. MATERIAL AND METHODS The human glioblastoma cell lines, LN229, U87-MG, U-251, U343, and the Hs683 glioma cell line were studied. The cell counting kit-8 (CCK-8) assay, cell cycle assay, wound-healing assay, transwell assay, Western blot, and quantitative real-time polymerase chain reaction (qRT-PCR) were used to evaluate cell proliferation, cell migration, and the cell cycle and expression of SALL1. Expression of SALL1 mRNA in 120 samples of cerebral glioma and 20 samples of normal brain were studied. Overall survival data from patients with cerebral glioma were analyzed. RESULTS SALL1 expression was down-regulated in human glioblastoma and glioma cells and in cerebral glioma tissues. Down-regulation of SALL1 expression was associated with reduced overall survival. Overexpression of SALL1 was associated with inhibition of cell proliferation associated with cell cycle arrest at the G0/G1 phase. SALL1 inhibited cell migration by preventing epithelial-mesenchymal transition (EMT) and down-regulating the expression of stem cell markers. Reduced levels of ß-catenin and downregulation of c-Myc and cyclin D1 and upregulation of p21and p27 expression were associated with SALL1 expression. CONCLUSIONS In human glioblastoma cells and cerebral glioma tissues, SALL1 acted as a tumor suppressor gene by inhibiting Wnt/ß-catenin signaling.

Photodynamic therapy combined with temozolomide inhibits C6 glioma migration and invasion and promotes mitochondrial-associated apoptosis by inhibiting sodium-hydrogen exchanger isoform 1.

OBJECTIVE: As a targeted therapeutic technique for glioma inhibition, photodynamic therapy (PDT) has gradually become a focus of basic research related to glioma treatment. The capacity of PDT to kill glioma cells involves varieties of pathways. In glioma cells, activated sodium-hydrogen exchanger isoform 1 (NHE1) can inhibit the cytotoxic effect of temozolomide (TMZ), promote cell migration and invasion, and inhibit cell apoptosis by changing the acid-base equilibrium. The purpose of our study was to explore if PDT combined with TMZ can effectively inhibit glioma cells by influencing NHE1 in vitro. METHODS: We analyzed the expression levels of proteins such as NHE1, ezrin, vimentin, Bcl-2, and Bax by Western blot analysis, we assessed the migration and invasion of rat C6 glioma cells by Transwell assay, and we evaluated C6 cell apoptosis in vitro by flow cytometry. RESULTS: Western blot results indicated that NHE1, ezrin and vimentin were downregulated after cotreatment of C6 cells, and intracellular acidification was detected by a fluorometric intracellular pH assay. The migration and invasion capacities of C6 cells were significantly hindered after cotreatment, as shown by the Transwell assay. Experimental data also revealed a significant increase in cell apoptosis after cotreatment, as detected by flow cytometry; corresponding proapoptotic changes in Bcl-2, Bax and caspase-3 were also observed in vitro. CONCLUSION: These results demonstrate that PDT combined with TMZ can inhibit C6 cell migration and invasion and promote mitochondrial-associated apoptosis by inhibiting NHE1. Therefore, this study provides supporting evidence for a potential method for the treatment of glioma.