AI Article Synopsis
- Histone acetylation plays a crucial role in regulating gene expression during development and cancer, with Trichostatin A (TSA) showing promise as a histone deacetylase inhibitor that can impede tumor growth.
- TSA effectively inhibits the proliferation of human oral squamous carcinoma cells (YD-10B) by causing growth arrest at the G2/M phase of the cell cycle and up-regulating p21waf while down-regulating Cyclin B1.
- The treatment with TSA leads to mitochondrial membrane damage, cytochrome c release, and activation of caspases, suggesting it triggers apoptosis in these cancer cells, highlighting its potential as a therapeutic agent against oral tumors.
Article Abstract
Histone acetylation is one of the key chromatin modifications that control gene transcription during development and tumorigenesis. Recently, it was reported that the histone deacetylase inhibitor, Trichostatin A (TSA), induces growth arrest and apoptosis in tumors. However, the molecular mechanisms responsible for its antitumor effects are not clear. The purpose of this study was to investigate the effect of TSA on human oral squamous carcinoma cells and to determine the mechanisms underlying the antitumor activity of TSA. MTT assays showed that TSA inhibited cell proliferation in YD-10B cells. TSA also effectively arrested cell cycle progression at the G2/M phase through the up-regulation of p21waf expression, down-regulation of Cyclin B1 and reduction of the inhibitory phophorylation of Cdc2. In addition, mitochondrial membrane destruction was induced by a 48 h TSA treatment. TSA also induced cytochrome c release and proteolytic activation of caspase 3 and caspase 7 in YD-10B cells. Taken together, these observations in YD-10B oral cancer cells reveal the potential value of TSA in inhibiting oral tumor growth.
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| http://dx.doi.org/10.3892/or.2011.1496 | DOI Listing |
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