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Long Noncoding MAGI2-AS3 Suppresses Several Cellular Processes of Lung Squamous Cell Carcinoma Cells by Regulating miR-374a/b-5p/CADM2 Axis

Authors He J, Zhou X, Li L, Han Z

Received 26 September 2019

Accepted for publication 17 December 2019

Published 15 January 2020 Volume 2020:12 Pages 289—302

DOI https://doi.org/10.2147/CMAR.S232595

Checked for plagiarism Yes

Review by Single-blind

Peer reviewer comments 3

Editor who approved publication: Dr Seema Singh


Jia He, 1, 2 Xiaoyun Zhou, 1, 2 Li Li, 1, 2 Zhijun Han 1, 2

1Department of Thoracic Surgery, Peking Union Medical College Hospital, Beijing 100730, People’s Republic of China; 2Graduate School of Peking Union Medical College, Chinese Academy of Medical Sciences, Beijing 100730, People’s Republic of China

Correspondence: Zhijun Han
Department of Thoracic Surgery, Peking Union Medical College Hospital, Graduate School of Peking Union Medical College, Chinese Academy of Medical Sciences, No. 1 Shuaifuyuan, Dongcheng District, Beijing 100730, People’s Republic of China
Email handi473984@163.com

Background: Lung squamous cell carcinoma (LUSC) accounts for approximately 30% of all lung cancers that possesses the highest occurrence and mortality in all cancer types. Long noncoding RNAs have been reported to modulate tumor development for several decades.
Aim of the Study: This research aims to investigate the role of MAGI2-AS3 in LUSC.
Methods: RT-qPCR tested genes (including MAGI2-AS3, miR-374a/b-5p and CADM2) expression. Cell proliferation was detected by colony formation and EdU assays. Cell migration and invasion were evaluated by transwell assay. Flow cytometry analysis of apoptotic cells and Western blot analysis on apoptosis-related genes were applied to measure cell apoptosis. Nuclear-cytoplasmic fractionation and FISH assay positioned MAGI2-AS3. The combination between miR-374a/b-5p and MAGI2-AS3 (or CADM2) was determined by luciferase reporter assay and RIP assay.
Results: MAGI2-AS3 inhibited the proliferative, migratory and invasive capability of LUSC cells with upregulated expression. Additionally, MAGI2-AS3 overexpression promoted cell apoptosis. We discovered that MAGI2-AS3 was located in the cytoplasm. Hereafter, we found out that MAGI2-AS3 targeted miR-374a/b-5p. CADM2 was targeted by miR-374a/b-5p. Finally, rescue assays indicated that the promoting effects of miR-374a/b-5p amplification on biological activities were restored by CADM2 addition.
Conclusion: In conclusion, lncRNA MAGI2-AS3 suppressed LUSC by regulating miR-374a/b-5p/CADM2 axis, which might potentially serve as a therapeutic marker for LUSC patients.

Keywords: lung squamous cell carcinoma, LUSC, MAGI2-AS3, miR-374a/b-5p, CADM2

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