Long Non-Coding RNA JPX Contributes to Tumorigenesis by Regulating miR-5195-3p/VEGFA in Non-Small Cell Lung Cancer
Authors Li G, Li X, Yuan C, Zhou C, Li X, Li J, Guo B
Received 24 March 2020
Accepted for publication 12 January 2021
Published 12 February 2021 Volume 2021:13 Pages 1477—1489
Checked for plagiarism Yes
Review by Single anonymous peer review
Peer reviewer comments 3
Editor who approved publication: Dr Beicheng Sun
Guanglian Li, Xinrui Li, Chao Yuan, Caifeng Zhou, Xinxin Li, Jinfang Li, Bin Guo
Department of Oncology, The People’s Hospital of Shouguang, Weifang, People’s Republic of China
Correspondence: Bin Guo
Department of Oncology, The People’s Hospital of Shouguang, No. 1223, Jiankang Street, Shouguang, Shandong, 262700, People’s Republic of China
Tel +86 536 5225033
Background: Lung cancer is the most frequently diagnosed cancer. Of all lung cancers, 80– 85% are verified as non-small-cell lung cancer (NSCLC). Just proximal to X-inactive specific transcript (JPX), functions as lncRNA, contributed to tumor progression and suggested a poor prognosis in NSCLC. However, the pathogenesis of JPX involved in NSCLC is still unclear.
Methods: The expressions of JPX, miR-5195-3p, and Vascular endothelial growth factor A (VEGFA) were detected by real-time quantitative polymerase chain reaction (RT-qPCR). Proliferation, colony number, apoptosis, invasion, and migration were analyzed by Cell Counting Kit-8 (CCK-8), colony formation, flow cytometry, transwell, and wound healing assays, severally. The protein levels of VEGFA, E-cadherin, N-cadherin, and Vimentin were detected by Western blot assay. The interaction between JPX, miR-5195-3p and VEGFA was predicted by starBase, and then verified by the dual-luciferase reporter, RNA Immunoprecipitation (RIP) and RNA pull-down assay. The biological role of JPX on NSCLC tumor growth was assessed by the xenograft tumor model in vivo.
Results: JPX and VEGFA were upregulated, and miR-5195-3p was downregulated in NSCLC. JPX induced proliferation, colony number, invasion, migration, epithelial–mesenchymal transition (EMT), and inhibited apoptosis of NSCLC cells. JPX is directly bound to miR-5195-3p. JPX regulated NSCLC cell proliferation, apoptosis and EMT by modulating miR-5195-3p. miR-5195-3p hindered NSCLC cells proliferation, EMT and accelerated apoptosis by directly targeting VEGFA. JPX silencing hindered the cell growth of NSCLC in vivo.
Conclusion: JPX facilitated proliferation, colony number, invasion, migration, EMT, and repressed apoptosis by miR-5195-3p/VEGFA axis, offering a possible therapeutic strategy for NSCLC.
Keywords: lncRNA JPX, miR-5195-3p, VEGFA, lung cancer, proliferation, apoptosis, EMT
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]