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Research Paper|Volume 13, Issue 21|pp 24339—24348

Deletion of miR-15a inhibited glioma development via targeting Smad7 and inhibiting EMT pathway

Yanfeng Guo1, Xiaopeng Gao1, Shien An1, Xin Li1, Lekun Pan1, Hongyan Liu2, Jixiang Liu1, Jianzhou Gao1, Zhihuang Zhao3, Gang Li3, Yonggang Han3, Yabin Li3, Zhisheng Ji3
  • 1Department of Neurosurgery, The First Hospital of Handan, Handan, Hebei Province, China
  • 2Department of E.N.T, The First Hospital of Handan, Handan, Hebei Province, China
  • 3Third Department of Neurosurgery, Cangzhou Central Hospital, Cangzhou, Hebei Province, China
Received: June 7, 2021Accepted: September 28, 2021Published: November 11, 2021
https://doi.org/10.18632/aging.203684

Copyright: © 2021 Guo et al. This is an open access article distributed under the terms of the Creative Commons Attribution License (CC BY 3.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.

Abstract

In the present study, we found the expression of miR-15a-5p (miR-15a) was increased in glioma tissues, and we further explore the underlying mechanism of miR-15a in glioma progression. Microarray analysis used to identify the differentially expressed microRNAs (miRNAs) in glioma tissues. The expression of miR-15a in glioma tissues and cell lines was tested by qRT-PCR. Luciferase assay was used to determine the binding between miR-15a and Smad7. Wound healing and transwell assay were used to examine the role of miR-15a/Smad7 in SHG139 cells. Western blot was used to detect the protein level of Smad7 and epithelial-mesenchymal transition (EMT) markers. A tumor formation model in nude mice was established to measure the role of miR-15a in vivo. MiR-15a was significantly increased in glioma tissues and cells, which indicated a poor prognosis of glioma patients. MiR-15a mimics induced miR-15a level in SHG139 cells, and promoted the malignancy of SHG139 cells, while miR-15a inhibitor showed the opposite effects. Luciferase assay indicated that Smad7 was the direct target of miR-15a, and Smad7 was down-regulated in glioma tissues. Functional experiments revealed that miR-15a inhibitor inhibited the EMT pathway and the migration and invasion of glioma cells, but the silencing of Smad7 reversed the effects of miR-15a inhibitor in EMT pathway and glioma progression. Finally, we performed animal experiments to verify the role of miR-15a in vivo. Present study showed that deletion of miR-15a inhibited the activation of EMT signaling via targeting Smad7, thus suppressed the tumorigenesis and tumor growth of glioma.