Effects of MIR143 host gene on epithelial-mesenchymal transition of non-small cell lung cancer cells
CONG Li
YUAN Gaofeng
WANG Xia
SONG Zhen
LIN Lili
CAO Zhugen
Abstract：Objective To investigate the effects of MIR143 host gene(MIR143HG)on epithelial-mesenchymal transition(EMT),proliferation,migration and invasion of non-small cell lung cancer(NSCLC)cells via regulation of Janus kinase(JAK)signaling.Methods Expression of MIR143HG in lung cancer tissues and cells was detected using a gene expression profile interaction analysis platform and real-time fluorescence quantitative PCR.NSCLC cells H1299 were cultivated.The experimental grouping and treatment protocols were as follows:(1)Control group,transfected with the pcDNA3.1 empty plasmid;(2)MIR143HG overexpression group,transfected with the pcDNA3.1-MIR143HG recombinant plasmid;(3)JAK inhibition group,transfected with the pcDNA3.1 empty plasmid and treated with a JAK pathway inhibitor;and(4)the MIR143HG overexpression+JAK activation group,transfected with the pcDNA3.1-MIR143HG plasmid and treated with a JAK pathway activator.Real-time fluorescence quantitative PCR and Western blot were used to detect the phosphorylation level of the JAK signaling pathway and the expression of EMT-related factors.Cell proliferation,migration,and invasion abilities were evaluated using cell counting kit-8,scratch assay,and Transwell assay.Results MIR143HG was under-regulated in NSCLC tissues and cell lines(P<0.05).Compared with the Control group,MIR143HG overexpression group and JAK inhibition group showed reduced cell proliferation,migration and invasion abilities,accompanied by decreased phosphorylation levels of the JAK signaling pathway,decreased expression of N-cadherin and vimentin,and increased expression of E-cadherin,with statistically significant differences(P<0.05).The abilities of proliferation,migration and invasion as well as EMT process of the MIR143HG overexpression+JAK activation group were enhanced compared to the MIR143HG overexpression group(P<0.05).Conclusion MIR143HG is downregulated in NSCLC,and elevation of MIR143HG delays NSCLC progression by inhibiting the JAK signaling pathway,suggesting that it may prove to be a novel therapeutic target for NSCLC.
Keywords：Non-small cell lung cancerMIR143 host geneInvasionMigrationJanus kinase signaling pathway
Publication Date：2025-07-28
Online Publishing Date：2025-10-17(First online date of this platform, not the publication date of the document)
Pages：6( 625-630 )