BackgroundGliomas are commonly malignant tumors that arise in the human central nervous system and have a low overall five-year survival rate. Previous studies reported that several members of Rab GTPase family are involved in the development of glioma, and abnormal expression of Rab small GTPases is known to cause aberrant tumor cell behavior. In this study, we characterized the roles of Rab21 (Rab GTPase 21), a member of Rab GTPase family, in glioma cells.MethodsThe study involved downregulation of Rab21 in two glioma cell lines (T98G and U87) through transfection with specific-siRNA. Experiments using the MTT assay, cell cycle analysis, apoptosis assay, real-time PCR and western blot were performed to establish the expression levels of related genes.ResultsThe results show that downregulation of Rab21 can significantly inhibit cell growth and remarkably induce cell apoptosis in T98G and U87 cell lines. Silencing Rab21 resulted in significantly increased expression of apoptosis-related proteins (caspase7, Bim and Bax) in glioma cells.ConclusionsWe inferred that Rab21 silencing can induce apoptosis and inhibit proliferation in human glioma cells, indicating that Rab21 might act as an oncogene and serve as a novel target for glioma therapy.

PurposeCancer stem cells have recently been thought to be closely related to tumor development and reoccurrence. It may be a promising way to cure malignant glioma by using glioma stem cell-targeted dendritic cells as a tumor vaccine. In this study, we explored whether pulsing dendritic cells with antigens of glioma stem cells was a potent way to induce specific cytotoxic T lymphocytes and anti-tumor immunity.Materials and MethodsCancer stem cells were cultured from glioma cell line U251. Lysate of glioma stem cells was obtained by the repeated freezing and thawing method. Dendritic cells (DCs) were induced and cultured from the murine bone marrow cells, the biological characteristics were detected by electron microscope and flow cytometry. The DC vaccine was obtained by mixing DCs with lysate of glioma stem cells. The DC vaccine was charactirizated through the mixed lymphocyte responses and cell killing experiment in vitro. Level of interferon-γ (IFN-γ) in the supernatant was checked by ELISA.ResultsAfter stimulation of lysate of glioma stem cell, expression of surface molecules of DC was up-regulated, including CD80, CD86, CD11C and MHC-II. DCs pulsed with lysate of glioma stem cells were more effective than the control group in stimulating original glioma cells-specific cytotoxic T lymphocytes responses, killing glioma cells and boosting the secretion of IFN-γ in vitro.ConclusionThe results demonstrated DCs loaded with antigens derived from glioma stem cells can effectively stimulate naive T cells to form specific cytotoxic T cells, kill glioma cells cultured in vitro.

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Background Glioma is the most common primary brain tumor and represents one of the most aggressive and lethal types of human cancer. BCL7 family has been found in several cancer types and could be involved in tumor progression. While the role of BCL7 family in human glioma has remained to be elucidated. Methods Paraffin-embedded tumor samples were obtained to detect BCL7 expression by performing in glioma. Data (including normalized gene expression and corresponding clinical data) were obtained from Gliovis, CGGA, GEO, cBioportal and Oncomine and were used to investigate BCL7 genes expression in glioma. Survival analyses were calculated by Kaplan–Meier methods and Cox regression analysis in TCGA and CGGA. Gene Set Enrichment Analyses (GSEA) and gene ontology (GO) analysis was employed to perform the biological processes enrichment. Results BCL7A expression in glioma tissues was lower compared to non-tumor brain tissues (NBT), and exhibited a negative correlation with glioma grades. Results from immunohistochemical (IHC) staining and public dataset validation demonstrated that BCL7B and BCL7C were highly expressed in glioma tissues compared to NBT. Cox regression analysis identified BCL7A as the only gene in the BCL7 family that was independently associated with the prognosis of lower-grade glioma (LGG) and glioblastoma (GBM). GO and GSEA analyses revealed the potential contribution of BCL7A in adaptive immune response and neutrophil activation in the tumor microenvironment. Moreover, we found that BCL7A had no prognostic effect on the overall survival of GBM patients who received IR only; however, patients who received chemotherapy (TMZ) combined with IR in the high BCL7A group survived longer than patients in the low BCL7A group (HR = 0.346, p < 0.05). Conclusion BCL7A is a new tumor suppressor gene and can be adopted as a biomarker for independent prognosis in glioma and to evaluate response to TMZ.