Non-Small Cell Lung Cancer

JPX[LncRNA]

miR-5195-3p[miRNA]

VEGFA[mRNA]

NSCLC cells

Homo sapiens (human)

Cancer Manag Res. 2021 Feb 12;13:1477-1489. doi: 10.2147/CMAR.S255317. eCollection 2021.

Long Non-Coding RNA JPX Contributes to Tumorigenesis by Regulating miR-5195-3p/VEGFA in Non-Small Cell Lung Cancer.

qPCR;RT-qPCR;RIP assay;RNA immunoprecipitation;RNA pull-down assay;Western blot;Flow Cytometry assay;RNA immunoprecipitation;RNA pull-down;

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.