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LncRNA TTN-AS1 Promotes Progression of Non-Small Cell Lung Cancer via Regulating miR-491-5p/ZNF503 Axis

Authors Qi G, Li L

Received 16 November 2019

Accepted for publication 19 March 2020

Published 1 July 2020 Volume 2020:13 Pages 6361—6371


Checked for plagiarism Yes

Review by Single anonymous peer review

Peer reviewer comments 2

Editor who approved publication: Dr Yao Dai

Guanbin Qi, Lei Li

Department of Respiratory and Critical Care Medicine, Huaihe Hospital, Henan University, Kaifeng, Henan 475000, People’s Republic of China

Correspondence: Lei Li
Department of Respiratory and Critical Care Medicine, Huaihe Hospital, Henan University, No. 115, Ximen Street, Kaifeng City, Henan Province 475000, People’s Republic of China
Tel +86-371-23906701

Background: Non-small cell lung cancer (NSCLC) is the most common type of lung cancer with high mortality worldwide. Long non-coding RNA (lncRNA) TTN antisense RNA1 (TTN-AS1) has been demonstrated to play a crucial role in a variety of cancers. This study was designed to investigate the function and molecular mechanism of lncRNA TTN-AS1 in NSCLC.
Methods: The expression levels of TTN-AS1, miR-491-5p and zinc finger protein 503 (ZNF503) were examined by quantitative real-time polymerase chain reaction (qRT-PCR) or Western blot assay, respectively. Cell viability was detected by 3-(4,5-dimethyl-2-thiazolyl)-2,5-diphenyl-2-H-tetrazolium bromide (MTT) assay. Cell migration and invasion were assessed by transwell assay. Epithelial-to-mesenchymal transition (EMT)-related proteins were measured using Western blot assay. The relationship between TTN-AS1, miR-491-5p and ZNF503 was predicted by starBase2.0 and confirmed by dual-luciferase reporter assay. Xenograft tumor experiment was conducted to analyze the tumor growth in vivo.
Results: The levels of TTN-AS1 and ZNF503 were up-regulated, while miR-491-5p expression was reduced in NSCLC tissues and cells. Knockdown of TTN-AS1 or ZNF503 suppressed cell proliferation, migration, invasion and EMT in NSCLC cells. Overexpression of ZNF503 reversed the effect of TTN-AS1 silencing on NSCLC progression. TTN-AS1 could modulate the expression of ZNF503 via sponging miR-491-5p. Furthermore, TTN-AS1 induced tumor growth in vivo.
Conclusion: Inhibition of TTN-AS1 hindered cell proliferation, migration, invasion and EMT in NSCLC cells by modulating miR-491-5p/ZNF503 axis, providing a promising biomarker for NSCLC treatment.

Keywords: TTN-AS1, miR-491-5p, ZNF503, progression, non-small cell lung cancer

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