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

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机构： [1]Department of Intervention, Tongren Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, 200336, China. [2]Department of Radiology, Ruijin Hospital Luwan Branch, Shanghai Jiao Tong University School of Medicine, No.149 Chongqing South Road, Shanghai, 200025, China. [3]Clinical Nuclear Medicine Center, Imaging Clinical Medical Center, Institute of Nuclear Medicine, Department of Nuclear Medicine, Shanghai Tenth People's Hospital, Tongji University School of Medicine, Shanghai, 200072, China. [4]Department of Operating Room, Tongji Hospital, Tongji University School of Medicine, Shanghai, 200065, China.

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关键词： Esophageal restenosis MIR503HG miR-16–5p FOSL1 EMT

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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.Copyright © 2025 The Authors. Published by Elsevier Inc. All rights reserved.

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出版当年[2025]版：

大类 | 3 区生物学

小类 | 2 区生物物理 3 区生化与分子生物学

最新[2025]版：

大类 | 3 区生物学

小类 | 2 区生物物理 3 区生化与分子生物学

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出版当年[2023]版：

Q1 BIOPHYSICS Q2 BIOCHEMISTRY & MOLECULAR BIOLOGY

最新[2024]版：

Q2 BIOPHYSICS Q3 BIOCHEMISTRY & MOLECULAR BIOLOGY

影响因子： 3 最新[2024版] 3.6 最新五年平均 3.8 出版当年[2023版] 3.8 出版当年五年平均 3.9 出版前一年[2022版] 3 出版后一年[2024版]

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第一作者机构： [2]Department of Radiology, Ruijin Hospital Luwan Branch, Shanghai Jiao Tong University School of Medicine, No.149 Chongqing South Road, Shanghai, 200025, China.

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