Circular RNA Circ_0016760 Modulates Non-Small-Cell Lung Cancer Growth Through the miR-577/ZBTB7A Axis
Authors Hao Y, Xi J, Peng Y, Bian B, Hao G, Xi Y, Zhang Z
Received 24 December 2019
Accepted for publication 21 May 2020
Published 8 July 2020 Volume 2020:12 Pages 5561—5574
Checked for plagiarism Yes
Review by Single anonymous peer review
Peer reviewer comments 2
Editor who approved publication: Dr Eileen O'Reilly
Yanhong Hao,1,* Junfeng Xi,1,* Yancai Peng,1 Burong Bian,2 Guangjun Hao,2 Yunfeng Xi,3 Zhibin Zhang1
1Department of Cardiothoracic Surgery, The First Hospital of Yulin, Yulin City, Shanxi Province, People’s Republic of China; 2Department of Oncology, The First Hospital of Yulin, Yulin City, Shanxi Province, People’s Republic of China; 3Department of Dermatological Surgery, The First Hospital of Yulin, Yulin City, Shanxi Province, People’s Republic of China
*These authors contributed equally to this work
Correspondence: Zhibin Zhang Email email@example.com
Background: Patients with locally advanced or metastatic non-small-cell lung cancer (NSCLC) have a poor prognosis. Circular RNA circ_0016760 (circ_0016760) is associated with the development of NSCLC. At present, the role and regulatory mechanism of circ_0016760 in NSCLC have not been well explained.
Methods: Quantitative real-time polymerase chain reaction (qRT-PCR) was executed to detect the expression of circ_0016760, miR-577, and Zinc finger and BTB domain containing 7A (ZBTB7A) mRNA in NSCLC tissues and cells. The colony formation, migration, invasion, and extracellular acidification rate (ECAR) of NSCLC cells were determined through colony formation, transwell, or ECAR assays. The relationship between circ_0016760 or ZBTB7A and miR-577 was analyzed via dual-luciferase reporter and RNA pull-down or RNA immunoprecipitation (RIP) assays. Protein level of ZBTB7A was evaluated with Western blot analysis. Xenograft assay was conducted to confirm the role of circ_0016760 in vivo.
Results: Circ_0016760 and ZBTB7A were upregulated and miR-577 was downregulated in NSCLC tissues and cells. Circ_0016760 exhaustion curbed the colony formation, migration, invasion, and ECAR of NSCLC cells in vitro and impeded tumor growth in vivo. Mechanically, circ_0016760 modulated ZBTB7A expression via sponging miR-577 in NSCLC cells. MiR-577 downregulation abolished the repressive effects of circ_0016760 silencing on colony formation, migration, invasion, and ECAR of NSCLC cells. Also, ZBTB7A upregulation overturned the repressive impacts of miR-577 elevation on colony formation, migration, invasion, and ECAR of NSCLC cells.
Conclusion: Circ_0016760 silencing impeded NSCLC advancement through regulation of the miR-577/ZBTB7A axis.
Keywords: circ_0016760, miR-577, ZBTB7A, NSCLC, ECAR
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