miR-139-5p Inhibits Lung Adenocarcinoma Cell Proliferation, Migration, and Invasion by Targeting MAD2L1

Li, Jianfeng and He, Xi and Wu, Xiaotang and Liu, Xiaohui and Huang, Yixiong and Gong, Yuchen and Huang, Tao (2020) miR-139-5p Inhibits Lung Adenocarcinoma Cell Proliferation, Migration, and Invasion by Targeting MAD2L1. Computational and Mathematical Methods in Medicine, 2020. pp. 1-10. ISSN 1748-670X

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Abstract

Background. miR-139-5p is lowly expressed in various human cancers and exerts its antitumor effect through different molecular mechanisms, yet the molecular mechanism of miR-139-5p in lung adenocarcinoma (LUAD) remains to be further elucidated. The study is aimed at investigating the role and the regulatory mechanism of miR-139-5p in LUAD progression. Methods. Differential analysis was performed on miRNA expression data in the TCGA-LUAD dataset. qRT-PCR was employed to detect the transcription levels of miR-139-5p and MAD2L1 in LUAD cells, while western blot was carried out for the detection of MAD2L1 protein expression. CCK-8 and Transwell assays were implemented to assess LUAD cell proliferation, migration, and invasion. A dual-luciferase reporter gene assay was conducted to verify the direct targeting relationship between miR-139-5p and MAD2L1. Results. miR-139-5p was significantly downregulated in LUAD cells in comparison with that in human normal bronchial epithelial cells. Overexpressing miR-139-5p inhibited LUAD cell proliferation, migration, and invasion, while opposite results could be observed when miR-139-5p was inhibited. MAD2L1 was identified as a direct target of miR-139-5p in LUAD. Besides, the inhibitory effect of miR-139-5p overexpression on LUAD cell proliferation, migration, and invasion was attenuated by overexpressing MAD2L1. Conclusion. Our study suggests that miR-139-5p is lowly expressed in LUAD cells and inhibits LUAD cell proliferation, migration, and invasion by targeted suppressing MAD2L1 expression. It is of potential significance for the prognosis and treatment of LUAD.

Item Type: Article
Subjects: Institute Archives > Medical Science
Depositing User: Managing Editor
Date Deposited: 02 Feb 2023 09:50
Last Modified: 02 Apr 2024 03:55
URI: http://eprint.subtopublish.com/id/eprint/1209

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