Hypoxia is an essential feature of the microenvironment of solid tumors, which 
regulates a variety of transcription factors including hypoxia-inducible 
factor-1α (HIF-1α). HIF-1α overexpression enhances tumor angiogenesis via 
upregulation of vascular endothelial growth factor (VEGF) and some other 
hypoxia-inducible angiogenic factors, which lead to a more aggressive tumor 
phenotype, tumor metastasis and resistance to radiation and chemotherapy. In 
this study, we found that a histone deacetylase (HDAC) inhibitor, trichostatin A 
(TSA), inhibited cell proliferation and invasion, blocked the cell cycle, and 
induced cell apoptosis in a dose- and time-dependent manner in the human tongue 
squamous cell carcinoma (TSCC) SCC-6 cell line in vitro. Furthermore, TSA 
reduced both basal levels and hypoxia-induced HIF-1α protein accumulation but 
not HIF-1α mRNA levels, and both protein and mRNA levels of VEGF expression. 
These results showed that TSA had a potent anticancer activity on TSCC cells, 
suggesting that TSA could be a promising drug targeting tumor angiogenesis via 
inhibition of HIF-1α and VEGF expression in the development of an effective 
chemopreventive and anticancer agent on human TSCCs.