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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

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