Abstract
BackgroundThe role of epithelial-mesenchymal transition (EMT) in the pathogenesis of keloids is currently raising increasing attention. Long noncoding RNAs (lncRNAs) govern a variety of biological processes, such as EMT, and their dysregulation is involved in many diseases including keloid disease. The aim of this study was to identify differentially expressed EMT-related lncRNAs in keloid tissues versus normal tissues and to interpret their functions.ResultsEleven lncRNAs and 16 mRNAs associated with EMT were identified to have differential expression between keloid and normal skin tissues (fold change > 1.5, P < 0.05). Gene Ontology (GO) analysis showed that these differentially expressed mRNAs functioned in the extracellular matrix, protein binding, the positive regulation of cellular processes, the Set1C/COMPASS complex and histone acetyltransferase activity. Kyoto Encyclopedia of Genes and Genomes (KEGG) analysis demonstrated that these mRNAs are involved in pathways in cancer. The lncRNA, XLOC_000587 may promote cell proliferation and migration by enhancing the expression of ENAH, while AF268386 may facilitate the invasive growth of keloids by upregulating DDR2.ConclusionsWe characterized the differential expression profiles of EMT-related lncRNAs and mRNAs in keloids, which may contribute to preventing the occurrence and development of keloids by targeting the corresponding signaling pathways. These lncRNAs and mRNAs may provide biomarkers for keloid diagnosis and serve as potential targets for the treatment of this disease.
Highlights
The role of epithelial-mesenchymal transition (EMT) in the pathogenesis of keloids is currently raising increasing attention
Transforming growth factor-β (TGF-β), connective tissue growth factor (CTGF), vascular endothelial growth factor (VEGF) and the renin–angiotensin system were reported to be potential targets in keloid management considering their participation in wound healing and keloid formation [3, 4]
A1–C1 refer to RNAs extracted from keloids, and A2–C2 refer to RNAs extracted from adjacent normal skin from the corresponding patients to enhance invasion and EMT in non-small cell lung cancer (NSCLC) cells [37], while Long noncoding RNA (lncRNA) H19 was found to facilitate the EMT and metastasis of esophageal cancer cells through the let-7c/STAT3/ EZH2/β-catenin axis [38]
Summary
The role of epithelial-mesenchymal transition (EMT) in the pathogenesis of keloids is currently raising increasing attention. Keloids are benign lesions with invasive growth beyond the original wound borders, in which the hyperproliferation of fibroblasts and excessive accumulation of extracellular matrix can be observed [1]. The contribution of epithelial-mesenchymal transition (EMT) to keloid overgrowth is appealing as a potential treatment target. EMT refers to the biological process associated with the loss of polarity of epithelial cells and their transformation into mesenchymal cells with migratory and invasive characteristics [7]. It has been reported that inflammatory stimuli and a hypoxic microenvironment may induce the transition from keratinocytes to fibroblasts, facilitating the invasive growth of keloids [8]
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