ArticleScientific reports2016
High mobility group box 1-induced epithelial mesenchymal transition in human airway epithelial cells.
Article in Scientific reports, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 44 papers.
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Who cites it
44 citing papers in PubMed, 66 citations in OpenAlex.
- HMGB1 mediates low-dose ionizing radiation-induced Wnt/β-catenin activation in SRA01/04 cells: Mechanistic clues to early cataractogenesis.International journal of molecular medicine · 2026Article
- Natural compounds and programmed necrosis: pioneering a new frontier in cancer treatments.Naunyn-Schmiedeberg's archives of pharmacology · 2025Review
- Berberine alleviates respiratory syncytial virus (RSV)-induced pediatric bronchiolitis and fibrosis via suppressing the HMGB1/TLR4/NF-κB pathway.Microbiology spectrum · 2025Article
- Matrix metalloproteinase-driven epithelial-mesenchymal transition: implications in health and disease.Journal of translational medicine · 2025Review
- The RNA-binding protein quaking is upregulated in nitrofen-induced congenital diaphragmatic hernia lungs at the end of gestation.Pediatric surgery international · 2024Article
- Sterile inflammation of peritoneal membrane caused by peritoneal dialysis: focus on the communication between immune cells and peritoneal stroma.Frontiers in immunology · 2024Review
- Impact of obesity on airway remodeling in asthma: pathophysiological insights and clinical implications.Frontiers in allergy · 2024Review
- C5a/C5aR1 axis as a key driver promotes epithelial-to-mesenchymal transition in airway epithelial cells in silica nanoparticles-induced pulmonary fibrosis.International immunopharmacology · 2023Article
- RAGE/SNAIL1 signaling drives epithelial-mesenchymal plasticity in metastatic triple-negative breast cancer.Oncogene · 2023Article
- Soluble receptors for advanced glycation end-products prevent unilateral ureteral obstruction-induced renal fibrosis.Frontiers in pharmacology · 2023Article
- Tetra-arsenic tetra-sulfide enhances NK-92MI mediated cellular immunotherapy in all-trans retinoic acid-resistant acute promyelocytic leukemia.Investigational new drugs · 2022Article
- Airway epithelial cell-specific deletion of HMGB1 exaggerates inflammatory responses in mice with muco-obstructive airway disease.Frontiers in immunology · 2022Article
- HMGA1, Moonlighting Protein Function, and Cellular Real Estate: Location, Location, Location!Biomolecules · 2021Review
- HN1L promotes migration and invasion of breast cancer by up-regulating the expression of HMGB1.Journal of cellular and molecular medicine · 2021Article
- The Epithelial-Immune Crosstalk in Pulmonary Fibrosis.Frontiers in immunology · 2021Review
- miR-200 family expression during normal and abnormal lung development due to congenital diaphragmatic hernia at the later embryonic stage in the nitrofen rat model.Pediatric surgery international · 2020Article
- GSK3 modulation in acute lung injury, myocarditis and polycystic kidney disease-related aneurysm.Biochimica et biophysica acta. Molecular cell research · 2020Review
- The differential effects of commercial specialized media on cell growth and transforming growth factor beta 1-induced epithelial-mesenchymal transition in bronchial epithelial cells.Molecular biology reports · 2020Article
- High-mobility group box-1 increases epithelial sodium channel activity and inflammation via the receptor for advanced glycation end products.American journal of physiology. Cell physiology · 2020Article
- The GSK‑3β/β‑catenin signaling pathway is involved in HMGB1‑induced chondrocyte apoptosis and cartilage matrix degradation.International journal of molecular medicine · 2020Article
Corrections and comments
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Authors and funding
8 authors at 4 institutions in 2 countries.
Funding
Abstract
Epithelial-mesenchymal transition (EMT) is implicated in bronchial remodeling and loss of lung function in chronic inflammatory airway diseases. Previous studies showed the involvement of the high mobility group box 1 (HMGB1) protein in the pathology of chronic pulmonary inflammatory diseases. However, the role of HMGB1 in EMT of human airway epithelial cells is still unclear. In this study, we used RNA sequencing to show that HMGB1 treatment regulated EMT-related gene expression in human primary-airway epithelial cells. The top five upregulated genes were SNAI2, FGFBP1, VIM, SPARC (osteonectin), and SERPINE1, while the downregulated genes included OCLN, TJP1 (ZO-1), FZD7, CDH1 (E-cadherin), and LAMA5. We found that HMGB1 induced downregulation of E-cadherin and ZO-1, and upregulation of vimentin mRNA transcription and protein translation in a dose-dependent manner. Additionally, we observed that HMGB1 induced AKT phosphorylation, resulting in GSK3β inactivation, cytoplasmic accumulation, and nuclear translocation of β-catenin to induce EMT in human airway epithelial cells. Treatment with PI3K inhibitor (LY294006) and β-catenin shRNA reversed HMGB1-induced EMT. Moreover, HMGB1 induced expression of receptor for advanced glycation products (RAGE), but not that of Toll-like receptor (TLR) 2 or TLR4, and RAGE shRNA inhibited HMGB1-induced EMT in human airway epithelial cells. In conclusion, we found that HMGB1 induced EMT through RAGE and the PI3K/AKT/GSK3β/β-catenin signaling pathway.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.