Circ_0020123 Increases ZFX Expression to Facilitate Non-Small Cell Lung Cancer Progression by Sponging miR-142-3p
Authors Lu J, Ma X, Lin J, Hou P
Received 3 December 2020
Accepted for publication 26 January 2021
Published 18 February 2021 Volume 2021:13 Pages 1687—1698
Checked for plagiarism Yes
Review by Single anonymous peer review
Peer reviewer comments 2
Editor who approved publication: Dr Seema Singh
Jiancong Lu,1,* Ximiao Ma,2,* Junhong Lin,1 Peifeng Hou3– 5
1Department of Respiratory Diseases, Huizhou Municipal Central Hospital, Huizhou, 516001, People’s Republic of China; 2Department of Thoracic Surgery, Central South University Xiangya School of Medicine Affiliated Haikou Hospital, Haikou, People’s Republic of China; 3Department of Oncology, Fujian Medical University Union Hospital, Fuzhou, 350001, Fujian, People’s Republic of China; 4Fujian Key Laboratory of Translational Cancer Medicine, Fujian Provincial Cancer Hospital, Fuzhou, 350001, Fujian, People’s Republic of China; 5Fujian Medical University Stem Cell Research Institute, Fujian Medical University, Fuzhou, 350001, Fujian, People’s Republic of China
*These authors contributed equally to this work
Correspondence: Peifeng Hou
Department of Oncology, Fujian Medical University Union Hospital, No. 29 Xinquan Road, Gulou District, Fuzhou City, Fujian Province, People’s Republic of China
Tel +86 13799987620
Background: Circular RNA (circRNA) is involved in the progression of various cancers and has been shown to be an important potential target for cancer therapy. Circ_0020123 has been found to act as oncogene to participate in the malignant progression of non-small cell lung cancer (NSCLC). Therefore, exploring new mechanisms of circ_0020123 regulating NSCLC progression will help us better understand its role in NSCLC.
Methods: Relative expression levels of circ_0020123, microRNA (miR)-142-3p, and zinc-finger protein X-linked (ZFX) in tissues and cells were determined by quantitative real-time PCR (qRT-PCR). Cell proliferation, apoptosis, migration and invasion were assessed using cell counting kit 8 (CCK8) assay, colony formation assay, flow cytometry and transwell assay. Western blot (WB) analysis was used to detect relative protein level. Besides, the interaction between miR-142-3p and circ_0020123 or ZFX was confirmed by dual-luciferase reporter assay and RNA immunoprecipitation (RIP) assay.
Results: Our results showed that circ_0020123 was upregulated in NSCLC, and its knockdown could suppress NSCLC cell proliferation, migration, invasion, and promote apoptosis. Circ_0020123 was found to interact with miR-142-3p. The inhibition effect of circ_0020123 silencing on NSCLC progression could be reversed by miR-142-3p inhibitor. ZFX could be targeted by miR-142-3p. The silencing of ZFX could hinder the progression of NSCLC and abolish the promotion effect of miR-142-3p inhibitor on NSCLC progression. In addition, circ_0020123 silencing inhibited NSCLC tumorigenesis by the miR-142-3p/ZFX axis.
Conclusion: These findings suggested that circ_0020123 might be a potential therapy target for NSCLC, which could promote NSCLC progression through regulating the miR-142-3p/ZFX axis.
Keywords: non-small cell lung cancer, circ_0020123, miR-142-3p, ZFX
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