Upregulation of miR-1825 inhibits the progression of glioblastoma by suppressing CDK14 though Wnt/[beta]-catenin signaling pathway

Background Mounting 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. Methods qRT-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, [beta]-catenin, c-myc, p-c-Jun). MTT and transwell assays were used for detecting GBM cell progression, including cell viability, migration, and invasion. Results The 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/[beta]-catenin signaling pathway in GBM development. Conclusion In conclusion, miR-1825 upregulation suppressed GBM progression by targeting CDK14 through Wnt/[beta]-catenin pathway. Keywords: miR-1825, CDK14, Glioblastoma, Wnt/[beta]-catenin