Abstract
BackgroundMounting evidences displayed that miRNAs play crucial roles in tumor initiation and development. However, the regulation and relevant mechanism of miR-1825 in glioblastoma (GBM) remain unclear.MethodsqRT-PCR was used to detect miR-1825 and CDK14 mRNA expression. Western blot was applied for testing protein levels (VEGF, E-cadherin, N-cadherin, vimentin, β-catenin, c-myc, p-c-Jun). MTT and transwell assays were used for detecting GBM cell progression, including cell viability, migration, and invasion.ResultsThe results showed that miR-1825 was decreased in GBM tissue specimens by qRT-PCR and it was confirmed as a prognostic marker of GBM by Kaplan-Meier survival analysis. Moreover, we also found that miR-1825 upregulation suppressed GBM cell viability, tumor growth, invasion, and migration. Furthermore, CDK14 was first identified as the direct target of miR-1825 by Luciferase reporter assay. CDK14 acted as an oncogene in GBM development by immunohistochemistry. In addition, Western blot analysis demonstrated that miR-1825 regulated Wnt/β-catenin signaling pathway in GBM development.ConclusionIn conclusion, miR-1825 upregulation suppressed GBM progression by targeting CDK14 through Wnt/β-catenin pathway.
Highlights
Glioblastoma (GBM) are tumors derived from neuroepithelial tumors, accounting for 40 to 50% of brain tumors [1, 2]
MiR-1825 downregulation was associated with poor prognosis Here, we detected miR-1825 expression in GBM tissue specimens
The findings displayed that expression of miR-1825 was downregulated in GBM tissues compared with that in normal tissues (Fig. 1a)
Summary
Glioblastoma (GBM) are tumors derived from neuroepithelial tumors, accounting for 40 to 50% of brain tumors [1, 2]. The Currently, miRNAs were determined as the potential in cancer treatment [5, 6] and it can modulate a tumor’s development and progression by regulating their target genes [7,8,9]. In GBM, many miRNAs have been proved to participate in cell progression and development. MiR-365 displayed the inhibitory effect on GBM cell viability and migration via targeting PAX6 [10]. MiR-210 was proved to inhibit GBM cell invasion and migration by targeting BNDF [11]. The regulation and relevant mechanism of miR-1825 in glioblastoma (GBM) remain unclear
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