Back to Journals » Cancer Management and Research » Volume 13

CircRNA ZNF609 Knockdown Represses the Development of Non-Small Cell Lung Cancer via miR-623/FOXM1 Axis

Authors Wang F, Li X, Jia X, Geng L

Received 15 September 2020

Accepted for publication 7 November 2020

Published 4 February 2021 Volume 2021:13 Pages 1029—1039

DOI https://doi.org/10.2147/CMAR.S282162

Checked for plagiarism Yes

Review by Single anonymous peer review

Peer reviewer comments 2

Editor who approved publication: Dr Yong Teng


Fanghan Wang,1 Xiangfeng Li,2 Xigao Jia,3 Luxin Geng1

1Department of Oncology, 4th People’s Hospital of Zibo, Zibo, Shandong, 255000, People’s Republic of China; 2Department of Radiology, 4th People’s Hospital of Zibo, Zibo, Shandong, 255000, People’s Republic of China; 3Department of Medicine, 4th People’s Hospital of Zibo, Zibo, Shandong, 255000, People’s Republic of China

Correspondence: Fanghan Wang
Department of Oncology, 4th People’s Hospital of Zibo, No. 210, Shanquan Road, Zhangdian District, Zibo, Shandong, 255000, People’s Republic of China
Tel +86-533-2982547
Email fanghanwang197406@163.com

Background: The dysregulated circular RNAs (circRNAs) are relevant to the development of non-small cell lung cancer (NSCLC). Nevertheless, the function and mechanism of circRNA zinc finger protein 609 (circZNF609) in NSCLC development remain uncertain.
Methods: Sixty-two NSCLC patients were recruited. circZNF609, microRNA-623 (miR-623) and forkhead box M1 (FOXM1) abundances were measured via quantitative reverse transcription polymerase chain reaction or Western blot. Cell viability, apoptosis, migration and invasion were analyzed via cell counting kit-8 (CCK8), flow cytometry, caspase3 activity, transwell assay and Western blot. The interaction between miR-623 and circZNF609 or FOXM1 was analyzed via dual-luciferase reporter analysis, RNA immunoprecipitation and pull-down. The function of circZNF609 on cell growth in vivo was tested via xenograft model.
Results: circZNF609 abundance was enhanced in NSCLC tissues and cells. High expression of circZNF609 indicated the lower overall survival. circZNF609 interference restrained cell viability, migration and invasion and increased apoptosis. miR-623 was targeted via circZNF609. FOXM1 was targeted via miR-623 and regulated via circZNF609. miR-623 knockdown or FOXM1 overexpression mitigated the role of circZNF609 silence in NSCLC development. circZNF609 knockdown decreased NSCLC xenograft tumor growth.
Conclusion: circZNF609 knockdown repressed NSCLC development via regulating miR-623 and FOXM1.

Keywords: non-small cell lung cancer, circZNF609, FOXM1, miR-623

Creative Commons License This work is published and licensed by Dove Medical Press Limited. The full terms of this license are available at https://www.dovepress.com/terms.php 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]