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Objective. To explore the mechanism of glioma from MYB family genes from the perspective of the circRNA-miRNA-mRNA regulatory network. Methods. First, the MYB family genes were analyzed by multiple bioinformatics analyses to identify one gene most associated with glioma. Then, the prognostic value and clinical characteristics of the gene were evaluated by bioinformatics analysis and experiments in glioma cells. Next, the target miRNA and circRNA were predicted and verified by dual-luciferase reporter assays. Besides, the functions of target circRNA in glioma were investigated by CCK-8 and Transwell assays. At last, the relation between the screened MYB gene, miRNA, and circRNA in glioma was identified by rescue experiments. Results. After expression and Cox and survival analysis of six MYB family genes, MYBL2 was identified as the gene most associated with glioma. Then, we found that MYBL2 expression in primary gliomas was higher than those in other histologies, and it had variable expression according to clinical features. Furthermore, MYBL2 knockdown in glioma cells impairs cell growth, invasion, and migration in functional studies. Then, miR-30e-5p and circFAT1(e2) were identified as targets of MYBL2 by bioinformatics prediction and experimental verification. Finally, the relationship between circFAT1(e2), MYBL2, and miR-30e-5p was elucidated by rescue experiments. Conclusion. circFAT1(e2) could promote glioma development by regulating MYBL2 and miR-30e-5p, and MYBL2 has diagnostic and prognostic values in glioma. [ABSTRACT FROM AUTHOR]

MicroRNAs (miRNAs) are small non-coding RNAs frequently dysregulated in human malignancies. In this study, we found that miR-181c was down-regulated both in glioblastoma tissues and cell lines. We also annotated 566 TCGA miRNA expression profiles and found that patients with high microRNA-181c (miR-181c)-expressing tumors had significantly longer OS and PFS. Overexpression of miR-181c evidently inhibited glioblastoma cell line T98G migration and invasion. Further, the expression of E-cadherin was significantly upregulated and that of N-cadherin and vimentin was significantly down-regulated. We also found that miR-181c overexpression inhibited TGF-β signaling by down-regulating TGFBR1, TGFBR2 and TGFBRAP1 expression. Overall, our study found that miR-181c plays a key role in glioblastoma cell invasion, migration and mesenchymal transition suggesting potential therapeutic applications. [ABSTRACT FROM AUTHOR]

Background Aberrant DNA methylation is associated with tumor onset and progression. Study has verified that the DNA methylation of miR-152 was mediated in many tumors, but whether it involved in glioblastomas was still unclear. Methods This study enrolled 20 patients with glioma to analyze the expression pattern of miR-152. Real-time PCR and western blot were used to detect the mRNA or protein expression level, respectively. The relationship between miR-152 and runx2 was detected by Luciferase reporter assay. The methylation level of miR-152 was determined by methylation-specific PCR. Cell proliferation and apoptosis were detected by MTT and Annexin-FITC/PI assay. Results The expression of miR-152 was down-regulated while the expression of DNMT1 was up-regulated in both glioma tissue and cell lines. MiR-152 was hypermethylated and its expression was negatively correlated with DNMT in glioma cell lines. DNMT1 knockdown promoted the expression of miR-152, however, DNMT1 overexpression suppressed the expression of miR-152. MiR-152 overexpression promoted glioma cell apoptosis while miR-152 knockdown promoted cell proliferation. MiR-152 targets Runx2 to regulate its expression, Runx2 overexpression abolished the effects of miR-152 overexpression. Conclusion MiR-152 regulated cell proliferation and apoptosis of glioma mediated by Runx2, while the mechanism of down regulated miR-152 in glioma tissues and cells was its hypermethylation. [ABSTRACT FROM AUTHOR]