Back to Journals » OncoTargets and Therapy » Volume 10

let-7d suppresses proliferation and invasion and promotes apoptosis of meningioma by targeting AEG-1

Authors Li H, Zhao J

Received 3 May 2017

Accepted for publication 28 June 2017

Published 6 October 2017 Volume 2017:10 Pages 4895—4904


Checked for plagiarism Yes

Review by Single-blind

Peer reviewers approved by Dr Amy Norman

Peer reviewer comments 3

Editor who approved publication: Dr Yao Dai

Hui Li, Jianmin Zhao

Department of Neurology, Xinxiang Central Hospital, Xinxiang, China

Background: let-7d has been indicated to act as a tumor suppressor in various cancers. However, the function and molecular mechanism of let-7d in meningioma progression have not been elucidated.
Materials and methods: Quantitative real-time polymerase chain reaction (qRT-PCR) was performed to detect the expression levels of let-7d and AEG-1 mRNA in meningioma tissues and cell lines. The protein level of AEG-1 was measured by Western blot analysis. MTT assay, Transwell invasion assay and flow cytometry analysis were carried out to determine the proliferation, invasion and apoptosis of IOMM-Lee and CH-157MN cells, respectively. Target gene of let-7d was verified by luciferase reporter analysis.
Results: let-7d expression was downregulated, and AEG-1 expression was upregulated in meningioma tumor tissues. let-7d overexpression suppressed proliferation and invasion and induced apoptosis in IOMM-Lee and CH-157MN cells. Moreover, AEG-1 was a direct target of let-7d. Restoration of AEG-1 expression reversed let-7d-mediated suppression of the proliferation and invasion and let-7d-induced apoptosis in IOMM-Lee and CH-157MN cells.
Conclusion: let-7d repressed proliferation and invasion and promoted apoptosis of meningioma cells by targeting AEG-1. The present study provided a better understanding of the meningioma pathogenesis and a promising therapeutic target for meningioma patients.

Keywords: let-7d, AEG-1, meningioma cells, therapeutic target

Creative Commons License This work is published and licensed by Dove Medical Press Limited. The full terms of this license are available at and incorporate the Creative Commons Attribution - Non Commercial (unported, v3.0) License. By accessing the work you hereby accept the Terms. Non-commercial uses of the work are permitted without any further permission from Dove Medical Press Limited, provided the work is properly attributed. For permission for commercial use of this work, please see paragraphs 4.2 and 5 of our Terms.

Download Article [PDF]  View Full Text [HTML][Machine readable]