Anti-invasive activity of histone deacetylase inhibitors via the induction of Egr-1 and the modulation of tight junction-related proteins in human hepatocarcinoma cells
Autor: | Yung Hyun Choi, Taeg Kyu Kwon, Sung Ok Kim, Gi-Young Kim, Il-Whan Choi, Jae Hun Cheong, Byung Tae Choi, Nam Deuk Kim |
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Rok vydání: | 2009 |
Předmět: |
Carcinoma
Hepatocellular Biology Biochemistry Tight Junctions chemistry.chemical_compound Downregulation and upregulation Growth factor receptor Cell Movement medicine Claudin-3 Humans Neoplasm Invasiveness Neoplasm Metastasis RNA Small Interfering Molecular Biology Cell Proliferation Early Growth Response Protein 1 Histone deacetylase 5 Liver Neoplasms Membrane Proteins Cell migration Sodium butyrate Hep G2 Cells General Medicine Transfection Molecular biology Neoplasm Proteins Histone Deacetylase Inhibitors Trichostatin A chemistry Cancer research Histone deacetylase medicine.drug |
Zdroj: | BMB Reports. 42:655-660 |
ISSN: | 1976-6696 |
DOI: | 10.5483/bmbrep.2009.42.10.655 |
Popis: | The potential anti-metastasis and anti-invasion activities of early growth response gene-1 (Egr-1) and claudin-3, a tight junction (TJ)-related protein, were evaluated using histone deacetylase (HDAC) inhibitors in human hepatocarcinoma cells. The results of wound healing and Transwell assays showed that HDAC inhibitors such as trichostatin A and sodium butyrate inhibited cell migration and invasion. HDAC inhibitors markedly induced Egr-1 expression during the early period, after which expression levels decreased. In addition, the down-regulation of snail and type 1 insulin-like growth factor receptor (IGF-1R) in HDAC inhibitor-treated cells induced the upregulation of thrombospondin-1 (TSP-1), E-cadherin and claudin-3. Cells transfected with Egr-1 and claudin-3 siRNA displayed significant blockage of HDAC inhibitor-induced anti-invasive activity. Collectively, these findings indicate that the up-regulation of Egr-1 and claudin-3 are crucial steps in HDAC inhibitor-induced anti-metastasis and anti-invasion. [BMB reports 2009; 42(10): 655-660] |
Databáze: | OpenAIRE |
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