STAT3/ miR-486 /CCL20 regulates the migration and invasion of human lung adenocarcinoma cells

Abstract

Abstract Lung adenocarcinoma (LUAD) was one of the most important subtypes of lung cancer, which had attracted much attention due to its high morbidity and mortality in tumors for a long time. Although the threat of LUAD to human health had been reduced due to the continuous upgrading and innovative medical methods, the 5-year survival rate of lung adenocarcinoma was less than a quarter. There was a growing need to better understand the molecular mechanisms that influence the development of LUAD. Using bioinformatics methods, we identified 95 genes that were significantly upregulated in LUAD cells compared to normal epithelial cells by differential analysis. These genes were involved in antigen processing and presentation, chemokine signaling pathway, IL-17 signaling pathway, Toll-like receptor signaling pathway, etc. Among them, CCL20 had attracted attention due to its close association with other up-regulated genes and its influence on the survival of LUAD patients. In this study, single-cell transcriptome analysis and basic experiments confirmed that CCL20 was significantly overexpressed in LUAD, and that the STAT3/ miR-486 /CCL20 axis regulated the vitality, invasion and apoptosis of LUAD cells.