Long non-coding RNA JPX contributes to tumorigenesis by regulating miR-5195-3p/VEGFA in non-small cell lung cancer

Abstract

specific transcript (JPX), functions as lncRNA, contributed to tumor progression and sug- gested 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-mesench- ymal 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.