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Original Research Article | OPEN ACCESS

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

Jianfeng Bai1, Qingqing Yu2, Tongbo Ning1

1Department of Neurosurgery; 2Department of Medicine, Weihai Central Hospital, Weihai City, Shandong Province, China.

For correspondence:-  Tongbo Ning   Email: 123110729@qq.com   Tel:+866313806624

Accepted: 26 June 2021        Published: 29 July 2021

Citation: Bai J, Yu Q, Ning T. Up-regulation of miR-30b suppresses glioblastoma by negatively regulating MEF2D through Wnt/β-catenin signaling pathway. Trop J Pharm Res 2021; 20(7):1325-1330 doi: 10.4314/tjpr.v20i7.1

© 2021 The authors.
This is an Open Access article that uses a funding model which does not charge readers or their institutions for access and distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/4.0) and the Budapest Open Access Initiative (http://www.budapestopenaccessinitiative.org/read), which permit unrestricted use, distribution, and reproduction in any medium, provided the original work is properly credited..

Abstract

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/β-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/β-catenin signaling pathways.
Conclusion: These results indicate the critical role of miR-30b/MEF2D axis in glioblastoma via EMT and Wnt/β-catenin pathways. Thus, the miR-30b/MEF2D axis might be a beneficial therapeutic target for the management of glioblastoma patients.

Keywords: MiR-30b, MEF2D, Glioblastoma, Wnt/?-catenin, EMT

Impact Factor
Thompson Reuters (ISI): 0.6 (2023)
H-5 index (Google Scholar): 49 (2023)

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