ArticleThe Journal of biological chemistry2017
Down-regulation of Claudin-2 Expression and Proliferation by Epigenetic Inhibitors in Human Lung Adenocarcinoma A549 Cells.
Article in The Journal of biological chemistry, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.
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Who cites it
27 citing papers in PubMed, 41 citations in OpenAlex.
- Arteannuin B Inhibits NSCLC Cells via Regulating miR-194-3p/CLDN2 Axis.Cancer medicine · 2026Article
- Claudins in Cancer: A Current and Future Therapeutic Target.International journal of molecular sciences · 2024Review
- The Roles and Regulatory Mechanisms of Tight Junction Protein Cingulin and Transcription Factor Forkhead Box Protein O1 in Human Lung Adenocarcinoma A549 Cells and Normal Lung Epithelial Cells.International journal of molecular sciences · 2024Article
- Expression of Cell-Adhesion Molecules inInternational journal of molecular sciences · 2023Article
- Article
- Claudin-4: A New Molecular Target for Epithelial Cancer Therapy.International journal of molecular sciences · 2023Review
- Anticancer Effects of Propolis Extracts Obtained Using the Cold Separation Method on Breast Cancer Cell Lines.Plants (Basel, Switzerland) · 2023Article
- Review
- Phenol-Rich Botanicals Modulate Oxidative Stress and Epithelial Integrity in Intestinal Epithelial Cells.Animals : an open access journal from MDPI · 2022Article
- Increase in Anticancer Drug-Induced Toxicity by Fisetin in Lung Adenocarcinoma A549 Spheroid Cells Mediated by the Reduction of Claudin-2 Expression.International journal of molecular sciences · 2022Article
- Hypomethylation ofInternational journal of molecular sciences · 2022Article
- Epithelial-mesenchymal transition: The history, regulatory mechanism, and cancer therapeutic opportunities.MedComm · 2022Review
- Anticancer Activity of Propolis and Its Compounds.Nutrients · 2021Review
- Effects of histone deacetylase inhibitors Tricostatin A and Quisinostat on tight junction proteins of human lung adenocarcinoma A549 cells and normal lung epithelial cells.Histochemistry and cell biology · 2021Article
- Use of four genes in exosomes as biomarkers for the identification of lung adenocarcinoma and lung squamous cell carcinoma.Oncology letters · 2021Article
- Article
- Down-Regulation of Claudin-2 Expression by Cyanidin-3-Glucoside Enhances Sensitivity to Anticancer Drugs in the Spheroid of Human Lung Adenocarcinoma A549 Cells.International journal of molecular sciences · 2021Article
- Rapid Clathrin-Mediated Uptake of Recombinant α-Gal-A to Lysosome Activates Autophagy.Biomolecules · 2020Article
- Article
- Mechanisms and Future of Non-Small Cell Lung Cancer Metastasis.Frontiers in oncology · 2020Review
Corrections and comments
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Claudin-2 is highly expressed in lung adenocarcinoma tissues and increases proliferation in adenocarcinoma cells. The chemicals that reduce claudin-2 expression may have anti-cancer effects, but such therapeutic medicines have not been developed. We found that azacitidine (AZA), a DNA methylation inhibitor, and trichostatin A (TSA) and sodium butyrate (NaB), histone deacetylase (HDAC) inhibitors, decrease claudin-2 levels. The effect of AZA was mediated by the inhibition of phosphorylated Akt and NF-κB. LY-294002, an inhibitor of phosphatidylinositol 3-kinase (PI3K), and BAY 11-7082, an NF-κB inhibitor, decreased claudin-2 levels. The reporter activity of claudin-2 was decreased by AZA and LY-294002, which was blocked by the mutation in a putative NF-κB-binding site. NF-κB bound to the promoter region of claudin-2, which was inhibited by AZA and LY-294002. AZA is suggested to decrease the claudin-2 mRNA level mediated by the inhibition of a PI3K/Akt/NF-κB pathway. TSA and NaB did not change phosphorylated Akt and NF-κB levels. Furthermore, these inhibitors did not change the reporter activity of claudin-2 but decreased the stability of claudin-2 mRNA mediated by the elevation of miR-497 microRNA. The binding of histone H3 to the promoter region of miR-497 was inhibited by TSA and NaB, whereas that of claudin-2 was not. These results suggest that HDAC inhibitors decrease claudin-2 levels mediated by the elevation of miR-497 expression. Cell proliferation was additively decreased by AZA, TSA, and NaB, which was partially rescued by ectopic expression of claudin-2. We suggest that epigenetic inhibitors suppress the abnormal proliferation of lung adenocarcinoma cells highly expressing claudin-2.
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