The lncRNA MIR503HG/miR-16-5p/FOSL1 pathway mediates autophagy to promote esophageal epithelial cells proliferation and EMT in esophageal restenosis.

Esophageal stents have been used increasingly to relieve malignant dysphagia and are widely employed in the treatment of esophageal stenosis. However, the clinical application of esophageal stents has been limited by esophageal restenosis. Our preliminary studies have indicated that long non-coding RNAs (lncRNAs) may be involved in the development of esophageal restenosis. The aim of this study was to investigate the role of the lncRNA MIR503HG (MIR503HG)/miR-16-5p/Fos-like antigen-1 (FOSL1) pathway in esophageal restenosis. We demonstrate that MIR503HG and FOSL1 expression levels were significantly upregulated, while miR-16-5p was decreased in hyperplastic esophageal tissues compared to normal controls. Knockdown of MIR503HG significantly repressed proliferation, extracellular matrix deposition, migration, epithelial-mesenchymal transition, autophagy, and promoted apoptosis in Het-1A cells, while MIR503HG overexpression had the opposite effect. Mechanistically, MIR503HG was found to competitively interact with miR-16-5p leading to increased FOSL1 expression. Taken together, our findings indicate that MIR503HG is involved in the development of esophageal restenosis through miR-16-5p-dependent regulation of FOSL1. Thus, targeting MIR503HG could be beneficial in the development of a novel targeted therapeutic strategy for esophageal restenosis.