Histone deacetylases (HDACs) are
enzymes that catalyze the removal of acetyl from
lysine residues in
histones and other
proteins, which results in gene transcriptional repression and subsequent changes in signaling events. HDACs inhibitors (HDACIs) have been used to reverse the aberrant epigenetic changes associated with
cancer. However, the effects of HDACIs on epithelial-mesenchymal transition (EMT) in human
cancer cells remain unclear. EMT is a fundamental process governing morphogenesis in multicellular organisms and promotes
cancer invasion and
metastasis. In this study, human
cancer cells were treated with the HDACI
trichostatin A (
TSA).
TSA was found to induce mesenchymal‑like morphological changes in BGC-823 human
gastric cancer and MCF-7
breast cancer cells, and increase the expression levels of the mesenchymal markers
Vimentin and Twist. However, the expression levels of the epithelial cell marker
E-cadherin were also increased in response to
TSA treatment, while cell migration was reduced by
TSA. Furthermore,
TSA decreased
cancer cell colony formation in BGC-823 and MCF-7 cells, and led to the deregulation of β-
catenin, a critical signaling molecule involved in EMT. In conclusion, the results suggested that
TSA exhibits dual functions in EMT induction and inhibition in human
cancer cells, but the detailed mechanisms require further investigation.