Back to Journals » Cancer Management and Research » Volume 13

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

Creative Commons License This work is published and licensed by Dove Medical Press Limited. The full terms of this license are available at 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]