Objective Lung squamous cell carcinoma(LUSC)is one of the most frequent malignant tumors in the world.Re-cent studies have shown that isoliquiritigenin(ISL)plays an anti-tumor role in tumor proliferation and metastasis.Therefore,this study aims to explore the mechanism of the role of ISL in anti-LUSC metastasis.Method Gradient concentrations of ISL were used to treat LUSC cells to explore the anticancer properties of ISL in the proliferation,migration and invasion of LUSC cells.Subsequently,bioinformatics methods were used to explore the possible interaction between long non-coding RNAs(ln-cRNA)MIR22HG/miR-24-3p/Fas ligand Gene(FASLG).Quantitative real-time polymerase chain reaction(qRT-PCR)was used to detect the expressions of lncRNA MIR22HG,miR-24-3p and FASLG in LUSC cells.Cell Counting Kit-8(CCK-8),clonal formation,scratch healing and Transwell assay were used to detect cell viability,proliferation,migration and in-vasion,respectively.The expression of epithelial-mesenchymal transition(EMT)and transfer-related proteins was detected by Western blot.The binding relationships between lncRNA MIR22HG and miR-24-3p,miR-24-3p and FASLG were verified by RNA Binding Protein Immunoprecipitation(RIP)assay and dual luciferase assay.Result ISL can significantly inhibit LUSC cell proliferation,migration and invasion.Biogenic analysis and clinical sample analysis showed that lncRNA MIR22HG was low expressed in LUSC,and ISL could inhibit the expression of lncRNA MIR22HG and the malignant behavior of LUSC cells.In ad-dition,lncRNA MIR22HG can regulate the expression of FASLG by sponge adsorption of miR-24-3p.The miR-24-3p was up-regulated in LUSC,and FASLG was down-regulated in LUSC.Over-expression of FASLG can reverse the promoting effect of miR-24-3p over-expression on LUSC proliferation,metastasis and EMT process.Conclusion These results suggest that ISL inhibits LUSC metastasis via the lncRNA MIR22HG/miR-24-3p/FASLG axis,suggesting that ISL has potential as a novel treatment for LUSC.
维普
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