Gliomas are the most common primary brain tumors with high mortality. The treatment for gliomas is largely limited due to its uncomprehending pathological mechanism. Here we aimed to investigate the effect of long noncoding RNA (lncRNA) coiled-coil domain-containing 26 (CCDC26) in glioma progression. In our study, the expression of CCDC26 was found upregulated in glioma tissues and cell lines compared with normal tissues and cell lines. Further exploration detected decreased cell proliferation and increased cell apoptosis in U-251 and M059J cells transfected with CCDC26-siRNA. In addition, the silencing of CCDC26 strongly reduced the wound closing rate and the number of invasive cells compared with the scramble group. Simultaneously, the expression of miR-203 was found suppressed in glioma tissues and cells lines. Suppressed level of miR-203 was then elevated in U-251 and M059J cells transfected with CCDC26-siRNA. The result of the luciferase activity assay also showed that the luciferase activity was strongly strengthened by adding the miR-203 inhibitor into the CCDC26 WT group. Moreover, CDCC26-siRNA counteracted the effect of the miR-203 inhibitor in facilitating cell viability and mobility in U-251 cells. The in vivo experiment also revealed that CCDC26-siRNA inhibited glioma growth and metastasis. Taken together, our research indicated a CCDC26/miR-203 pathway in regulating the growth and metastasis of gliomas, providing new viewpoints and promising targets for glioma therapy.

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Epithelial–mesenchymal transition (EMT) plays a pivotal role in cancer progression. Hsa-miR-205 is considered one of the fundamental regulators of EMT. In the present study, we found that miR-205 was down-regulated in glioma tissues and human glioma cells U87 and U251. Meanwhile, miR-205 overexpression enhanced E-cadherin, reduced mesenchymal markers, and decreased cell proliferation, migration, and invasion in vitro. In vivo, miR-205 suppressed tumor growth. Additionally, HOXD9 was confirmed as a direct target of miR-205. Suppression of HOXD9 by miR-205 was demonstrated by luciferase reporter assay, quantitative real time-PCR analysis, and western blot. Moreover, we observed a negative correlation between miR-205 and HOXD9 in human glioma tissues. In summary, our findings demonstrated that miR-205 suppresses glioma tumor growth, invasion, and reverses EMT through down-regulating its target HOXD9.

Recently, microRNA-133a (miR-133a) has been found to function in many diseases in previous studies, yet few studies have been focused on its role in glioma. This study aims to investigate the mechanism of miR-133a/CTGF on regulating the malignant phenotypes of glioma cells via the JAK/STAT signaling pathway. Sixty-five human glioma specimens were collected and 30 normal brain tissues were selected as controls. The expression of connective tissue growth factor (CTGF) and miR-133a in tissues was detected, and the relationship between their expression and the clinicopathological features as well as prognosis of glioma was analyzed. MiR-133a and CTGF expression in U87, A172, and HEB cell lines was determined. The expression of CTGF, signaling pathway-, proliferation-, migration-, invasion-, apoptosis-and epithelial-mesenchymal transition (EMT)-related factors was detected. A number of assays were used to detect cell proliferation, migration, invasion, cell cycle, apoptosis, glioma growth, and the targeting site between CTGF and miR-133a. MiR-133a was downregulated and CTGF was upregulated in human glioma tissues and cells. MiR-133a and CTGF expression was related to glioma's WHO staging and size. Downregulated miR-133a and upregulated CTGF caused unfavorable prognosis in glioma. Upregulated miR-133a suppressed CTGF expression and the activation of JAK/STAT signaling pathway, thereby constraining cell colony formation, proliferation, migration and invasion, and promoting apoptosis in glioma. Our study reveals that upregulated miR-133a and downregulated CTGF suppress cell proliferation, migration, and invasion in human glioma through the inhibition of the JAK/STAT signaling pathway.

Protein phosphatase 4 catalytic subunit (PP4C) has been identified to be overexpressed in various solid cancers. However, to date, the role of PP4C in glioma remains elusive. In the present study, we aimed to detect PP4C expression in glioma patients and explore its function in glioma and prognostic significance in patients with glioma. The expression levels of PP4C mRNA and protein in 30 glioma tissue specimens and 10 non-cancerous brain tissue specimens were detected by qRT-PCR and Western blot analysis. Moreover, immunohistochemistry was performed to assess PP4C expression in 120 glioma patients. The effects of siRNA-mediated PP4C silencing on the proliferation, migration, and invasion of U251 and U87 glioma cells were assessed. We found that PP4C was upregulated in glioma tissue at both mRNA and protein levels compared with non-cancerous brain tissue. Univariate and multivariate analyses indicated that high PP4C expression was an independent prognostic factor for poor survival of glioma patients. Knockdown of PP4C reduced the proliferation, migration, and invasion of U251 and U87 cells. In conclusion, our findings suggest that PP4C plays an oncogenic role in glioma development and progression and might serve as a prognostic biomarker as well as a potential therapeutic target for glioma.