Our results demonstrate that the MIR155HG/miR-155 axis plays a critical role in facilitating glioma progression and serves as a prognostic factor for patient survival in glioblastoma. High-throughput screening indicated that the MIR155HG/miR-155 axis inhibitor NSC141562 may be a useful candidate anti-glioma drug.

Abstract. Aim: To investigate the effect of moesin expression on cell proliferaton and invasion of human glioblastoma cell lines in vitro. Materials and Methods: Glioblastoma LN229 and U87 cells were transfected with the H4645-plenti-EGFP-moesin expression vector for moesin up-regulation. Moesin and β-catenin expression levels in the transfectedGlioblastoma is a highly invasive recalcitrant cancer that is poorly understood (1-9). Moesin is a member of the ezrinradixin-moesin (ERM) protein family and is a link between the actin cytoskeleton and the plasma membrane. Moesin is involved in cell morphology, motility and adhesion, as well as other processes of tumorigenesis (10-12). Moesin has been studied in estrogen receptor (ER)-negative breast cancers (13), basal breast carcinomas (14), pancreatic cancer (15), melanoma (16), and gastric carcinoma (17). Moesin expression correlated with pathologic grade and poor clinical outcome, including survival in astrocytoma (18,19). However, the role of moesin in human glioblastoma progression is incompletely understood and, thus, the topic of the present report.In this study, we investigated moesin's effect on the growth and invasion ability of the glioblastoma cells by upregulation of the gene (MSN). Materials and MethodsCell culture. The glioblastoma cell line LN229 and U87 were purchased from the Shanghai cell bank of the Chinese Academy of Sciences (Shanghai, China). The cells were cultured in RPMI 1640 medium (GIBCO Life Technologies, Grand Island, NY, USA) containing 10% fetal bovine serum (Thermo Fisher Scientific, Waltham, MA, USA), 100 U/ml penicillin and 100 μg/ml streptomycin (Thermo Fisher Scientific) at 37˚C with 5% CO 2 .Moesin-expression vector transfection. The H4645-plenti-enhanced green fluorescent protein (EGFP)-moesin expression vector was used for up-regulation of the moesin gene (MSN) in the LN229 and U87 glioblastoma cells (LN229-H4645 and U87-H4645, respectively). The H149 plenti-EGFP empty vector was used as negative control (LN229-H149 and U87-H149, respectively). The moesin expression vector was constructed by Obio Technology Corp., Ltd. (Shanghai, China). Cultured glioblastoma LN229 and U87 cells were transfected with the moesin expression vector according to the manufacturer's instructions. After 24h transfection, the medium was changed. Cells were then observed under fluorescence microscopy at 48 hours after transfection. Cells were selected and treated with 500-800 μg/ml G148 (Micropoly Biotech Co., Ltd, Nanjing, China) for 1 week. Images were obtained from fluorescence microscopy. Transfection efficiency of the expression vector in the two cell lines was 2211 This article is freely accessible online.

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Background/aimGlioma is the most common and malignant nervous system tumor and is associated with high-grade malignancy and high recurrence. The mammalian Dachshund1 (DACH1) is a recognized anti-tumor site and has low expression in several malignant tumors, including glioma. We designed and conducted this study to further determine the mechanism of DACH1 in glioma.Patients and methodsThe data collected from specimens of patients with glioma from GSE16011 and REMBRANDT databases were analyzed. The effect of DACH1 on proliferation, migration, and invasion of U87 and U251 cell lines was analyzed in vitro. The symbol targets of the Wnt/β-catenin pathway were also evaluated through Western blot.ResultsDACH1 deficiency was found in glioma tissues, and the DACH1 level was negatively correlated with the tumor malignancy. DACH1 overexpression inhibited the tumor proliferation, migration, and invasion. High expression of DACH1 also dampened the Wnt/β-catenin pathway, and the activation of the Wnt/β-catenin pathway partly led to the limited proliferation in glioma cells.ConclusionDownregulation of DACH1 was related to the malignancy and poor prognosis of patients with glioma, and DACH1 overexpression inhibited the tumor proliferation via the Wnt/β-catenin pathway. These findings might assist in the discovery of novel potential diagnostic and therapeutic targets for DACH1, thereby reducing the malignancy and recurrence of glioma.