Up-regulation of miR-30b suppresses glioblastoma by negatively regulating MEF2D through Wnt/-catenin signaling pathway

Purpose: To study miR-30b' significance on glioblastoma, and its underlying mechanism of action. Methods: Reverse transcription-quantitative polymerase chain reaction (RT-qPCR) while 3-(4,5)-dimethylthiahiazo (-z-y1)-3,5-di- phenytetrazoliumromide (MTT), Transwell, and xenograft tumor formation assays were carried out to study miR-30b's effect on glioblastoma while luciferase reporter assay was employed to study the interaction between MEF2D and miR-30b. Glioblastoma cells treatment with miR-30 mimic or inhibitor were subjected to Western blot assay to study the effect of Wnt/beta-catenin signaling on miR-30b/MEF2D axis-mediated cell progression. Results: MiR-30b was lowly expressed in glioblastoma tissues (p = 0.007), and this was associated with poor prognosis of patients (p = 0.022). The direct target of miR-30b was identified as MEF2D (p = 0.036). Increasing miR-30b blocked MEF2D expression in glioblastoma cells (p = 0.029). Moreover, MEF2D overturned miR-30b' inhibitory effect on glioblastoma cell progression (p = 0.041; p = 0.006; p = 0.037). In vivo, restoration of miR-30b inhibited tumor growth (p = 0.01) and MEF2D. Interestingly, restoration of miR-30b inhibited epithelial-to-mesenchymal transition (EMT) and Wnt/beta-catenin signaling pathways. Conclusion: These results indicate the critical role of miR-30b/MEF2D axis in glioblastoma via EMT and Wnt/beta-catenin pathways. Thus, the miR-30b/MEF2D axis might be a beneficial therapeutic target for the management of glioblastoma patients.