MiR-3918 Inhibits Tumorigenesis of Glioma via Targeting EGFR to Regulate PI3K/AKT and ERK Pathways
- 13 January 2022
- journal article
- research article
- Published by Springer Science and Business Media LLC in Journal of Molecular Neuroscience
- Vol. 72 (2), 433-440
- https://doi.org/10.1007/s12031-021-01952-1
Abstract
Increasing evidence has demonstrated the miRNAs’ action in cancerogenesis and tumor progression. Here, we explored the role and underlying mechanism of miR-3918 during glioma malignancy. miR-3918 and EGFR expression was detected in glioma tissues and tissues by RT-qPCR. The proliferative and migratory rate of glioma cells was assessed through CCK8 and Scratch wound-healing migration assay. Xenograft tumor mouse models were established for in vivo verification. A series of bioinformatics analysis coupled with luciferase reporter assays verified the targeted binding between miR-3918 and EGFR. Expression analyses demonstrated that miR-3918 was poorly expressed in glioma tissues while EGFR abundantly expressed. MiR-3918 overexpression impaired the proliferative and migratory capacities of glioma cells by inactivating PI3K/AKT and ERK pathways. Meanwhile, miR-3918 overexpression also retarded the growth of glioma xenograft. Mechanically, miR-3918 targeted EGFF which was further validated by the correlation of miR-3918 and EGFR expression in glioma tissues. When overexpressed, EGFR can restore the inactivated PI3K/AKT and ERK pathways caused by miR-3918 and influence the glioma cell proliferation and migration. Our findings are the first report that miR-3918/EGFR axis arrested the tumorigenesis of glioma via regulating PI3K/AKT and ERK pathways.Keywords
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