Dysregulation of microRNAs (miRNAs) is actively involved in the development and progression of glioma. miR-520c was previously found to inhibit glioblastoma cell migration. However, the clinical significance of miR-520c and its biological function in glioma remain largely unknown. In the present study, we found that miR-520c expression in glioma tissues was significantly decreased compared to adjacent non‑cancerous tissues. The low level of miR-520c was prominently correlated with advanced World Health Organization (WHO) grade and decreased overall survival of glioma patients. Overexpression of miR-520c in U251 cells significantly decreased the migration and invasion of the cancer cells, while miR-520c silencing promoted U87 cell migration and invasion in vitro. Mechanistically, miR-520c inversely regulated transforming growth factor-β receptor type 2 (TGFBRII) abundance in the glioma cells. Herein, TGFBRII was found to be a downstream target of miR-520c in glioma. Furthermore, an inverse correlation between TGFBRII and miR-520c expression was observed in the glioma cases. In constrast, restoration of TGFBRII expression abrogated the effects of miR-520c overexpression in U251 cells with increased cell migration and invasion. In addition, miR-520c overexpression blocked TGF-β1‑induced cell migration and invasion in U251 cells. Collectively, miR-520c may serve as a prognostic predictor and a therapeutic target for glioma patients.

Background: Gliomas are the most common type of primary tumors in the central nervous system. This study aimed to investigate the biological role of miR-410-3p in glioma and elucidate the potential molecular mechanisms involved. Methods: The expression levels of miR-410-3p in clinical tissue samples and glioma cell lines were determined using qRT-PCR analysis. The clinical significance of miR-410-3p in glioma was evaluated using Kaplan-Meier survival analysis and Fisher's exact test. The effects of miR-410-3p on glioma cell proliferation, apoptosis, migration and invasion were investigated using MTT assays, flow cytometry, transwell migration and invasion assays. Besides, corresponding mechanistic studies were carried out. Results: miR-410-3p was significantly down-regulated in glioma tissues. Besides, Kaplan-Meier analysis demonstrated that patients with low miR-410-3p expression had a shorter overall survival. Decreased miR-410-3p expression was associated with larger tumor size, lower Karnofsky performance score (KPS), and higher World Health Organization (WHO) grade. Over-expression of miR-410-3p suppressed cell proliferation, migration, and invasion, and accelerated apoptosis; whereas depletion of miR-410-3p facilitated cell proliferation, migration, and invasion, and inhibited apoptosis. Mechanistic investigations demonstrated that Ras-related protein 1A (RAP1A) was a direct target of miR-410-3p, and that rescue of RAP1A expression reversed miR-410-3p over-expression-induced inhibitory effects on cell proliferation, migration, and invasion. Notably, miR-410-3p over-expression repressed tumor growth in mouse xenograft models. Conclusion: Our findings indicate that miR-410-3p functions as a tumor suppressor in glioma by directly targeting RAP1A. Thus, this study may provide some new insights into gliomagenesis and progression.

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Recent studies have demonstrated that cytokines play an important role in the pathogenesis of intracranial aneurysm (IA). Tumor necrosis factor-α (TNF-α) is an important proinflammatory cytokine, which was shown to influence the development of IA, but there is no research data from China. Hence, the purpose of this study was to explore the relationship between TNF-α polymorphisms and IA in China. The association of genetic variants of TNF-α gene expression was investigated in a Chinese population with IA. The TNF-α-3959T>C(rs1799964), 4127C>A(rs1800630), 4133C>T(rs1799724), 4184C>T(rs4248158), and 4752G>A(rs361525) gene polymorphisms in 192 IA cases and 112 controls were analyzed using polymerase chain reaction (PCR). Differences in genotype and allele frequencies between patients and controls were tested. There were no significant differences in 4127C>A (p = 0.072), 4133C>T (p = 0.373), 4184C>T (p = 0.749), and 4752G>A (p = 0.184) genotype frequencies between the IA group and the control group. But this case-control association study revealed that TNF-α-3959T>C (p < 0.001) was significantly associated with increased risk of IA. These results suggested that a novel TNF-α locus was found to be closely correlated with the occurrence of IA in Chinese.