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miR-503 Inhibits Proliferation, Migration, And Angiogenesis Of Glioma By Acting On VEGFA Through Targeting LRIG2

Authors Sun SL, Shu YG, Tao MY

Received 10 July 2019

Accepted for publication 4 November 2019

Published 19 December 2019 Volume 2019:11 Pages 10599—10608

DOI https://doi.org/10.2147/CMAR.S222681

Checked for plagiarism Yes

Review by Single-blind

Peer reviewer comments 2

Editor who approved publication: Dr Alexandra R. Fernandes


Sheng-Li Sun, Yu-Gao Shu, Mei-Yi Tao

Department of Neurosurgery, Hunan Provincial People’s Hospital, Changsha 410005, People’s Republic of China

Correspondence: Mei-Yi Tao
Department of Neurosurgery, Hunan Provincial People’s Hospital, No. 61, Jiefang West Road, Changsha 410005, Hunan Province, People’s Republic of China
Tel +86 137 2389 3781
Email taomeiyirqc@163.com

Background: Glioma is a common malignant tumor of the human central nervous system, and the pathological characteristics include invasive growth, angiogenesis, and so on. Ectopic expression of miR-503 works as a critical factor in cancer cell proliferation, migration, and capillary-like tube formation. The potential mechanisms of miR-503 in angiogenesis of glioma cells are still not reported.
Methods: The expression levels of miR-503, LRIG2, and VEGFA mRNA and protein were performed by quantitative reverse transcription-PCR or Western blot assay. Dual-Luciferase reporter gene assay was used to determine the interaction between miR-503 and LRIG2. The concentration of VEGFA was measured using the ELISA method. The cell proliferation, migration, and angiogenesis of cocultured HCMEC/D3 cells were analyzed by MTT assay, transwell detection, and tube formation assay, respectively.
Results: The expression levels of LRIG2 and VEGFA were reduced in glioma cells with miR-503 overexpression and enhanced with miR-503 inhibition. Moreover, cell proliferation, migration, and angiogenesis of cocultured HCMEC/D3 cells were alleviated with miR-503 mimics transfection. VEGFA and miR-503 inhibitor promoted cell proliferation, cell migration, and angiogenesis. Luciferase reporter gene assay revealed that miR-503 could directly target LRIG2. Furthermore, knockdown of LRIG2 or addition of VEGF inhibitor bevacizumab could abrogate the effect of miR-503 inhibitor on VEGFA expression, as well as the promotion of cell proliferation, migration, and angiogenesis.
Conclusion: MiR-503 mediated LRIG2 suppression and regulated the expression of VEGFA, thereby reducing cell proliferation, migration, and angiogenesis of glioma cells. These results provide new insight into the action mechanism of miR-503-modulated signaling pathway in angiogenesis of glioma cells.

Keywords: glioma, miR-503, LRIG2, VEGFA, angiogenesis

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