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
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
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
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