ArticleLung2015
Regulation of Gene Expression by Sodium Valproate in Epithelial-to-Mesenchymal Transition.
Article in Lung, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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Who cites it
16 citing papers in PubMed, 26 citations in OpenAlex.
- CellMiner cross-database (CellMinerCDB) version 2.2 for explorations of patient-derived cancer cell line pharmacogenomics.Nucleic acids research · 2026Article
- Sirtuin 2 Exerts Regulatory Functions on Radiation-Induced Myocardial Fibrosis in Mice by Mediating H3K27 Acetylation of Galectin-3 Promoter.Acta Cardiologica Sinica · 2024Article
- Histone deacetylases: potential therapeutic targets for idiopathic pulmonary fibrosis.Frontiers in cell and developmental biology · 2024Review
- The mechanism of gut-lung axis in pulmonary fibrosis.Frontiers in cellular and infection microbiology · 2024Review
- Identification of AGR2 Gene-Specific Expression Patterns Associated with Epithelial-Mesenchymal Transition.International journal of molecular sciences · 2022Article
- Targeting Histone Deacetylases in Idiopathic Pulmonary Fibrosis: A Future Therapeutic Option.Cells · 2022Review
- HDAC Inhibition with Valproate Improves Direct Cytotoxicity of Monocytes against Mesothelioma Tumor Cells.Cancers · 2022Article
- Gut microbiome and metabolites: The potential key roles in pulmonary fibrosis.Frontiers in microbiology · 2022Review
- Pretreatment with valproic acid alleviates pulmonary fibrosis through epithelial-mesenchymal transition inhibition in vitro and in vivo.Laboratory investigation; a journal of technical methods and pathology · 2021Article
- More than a Genetic Code: Epigenetics of Lung Fibrosis.Molecular diagnosis & therapy · 2020Review
- Review
- Article
- HDAC inhibitors as antifibrotic drugs in cardiac and pulmonary fibrosis.Therapeutic advances in chronic disease · 2019Review
- Reactive Oxygen Species Drive Epigenetic Changes in Radiation-Induced Fibrosis.Oxidative medicine and cellular longevity · 2019Review
- Residual Ammonium Persulfate in Nanoparticles Has Cytotoxic Effects on Cells through Epithelial-Mesenchymal Transition.Scientific reports · 2017Article
- Article
Corrections and comments
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Authors and funding
7 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
purposeEpithelial-to-mesenchymal transition (EMT) is an important mechanism in cancer metastasis and pulmonary fibrosis. Previous studies demonstrated effect of histone H3 and H4 acetylation in cancer and pulmonary fibrosis, so we hypothesized that histone modification might play a crucial role in gene regulation during EMT. In this study, we investigated the mechanism behind EMT by analyzing comprehensive gene expression and the effect of sodium valproate (VPA), a class I histone deacetylase inhibitory drug, on histone modification.
methodsEMT was induced in human alveolar epithelial cells (A549) using 5 ng/mL of transforming growth factor (TGF)-β1. Various concentrations of VPA were then administered, and Western blotting was used to analyze histone acetylation or methylation. Comprehensive gene expression analysis was carried out by RNA sequencing, and chromatin immunoprecipitation was performed with an anti-acetyl histone H3 lysine 27 antibody.
resultsTGF-β1 stimulation led to a decrease in histone acetylation, especially that of histone H3K27, and H3K27ac localization was decreased at particular gene loci. This decrease was recovered by VPA treatment, which also up-regulated the mRNA expression of genes down-regulated by TGF-β1, and correlated with the localization of H3K27ac. However, genes up-regulated by TGF-β1 stimulation were not suppressed by VPA, with the exception of COL1A1.
conclusionsHistone acetylation was down-regulated by TGF-β1 stimulation in A549 cells. VPA partially inhibited EMT and the decrease of histone acetylation, which plays an important role in the progression of EMT.
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