Abstract
Histone acetyltransferase GCN5 is a critical component of the TGF-β/Smad signaling pathway in breast cancer cells; however, it remains unknown whether it is involved in the development and progression of breast cancer. The present study investigated the role of GCN5 in the induction of the EMT by TGF-β1 in breast cancer cells and its underlying molecular mechanism of action. GCN5 activity was elevated and GCN5 mRNA expression and protein expression were increased in MDA-MB231 cells following stimulation with TGF-β1. Furthermore, TGF-β1 stimulation decreased expression of the epithelial cell marker E-cadherin and increased expression of the mesenchymal cell markers, N-cadherin and vimentin, as well as the expression of other EMT markers, including snail and slug. However, these changes were reversed following GCN5 knockdown leading to the downregulation of GCN5 expression. GCN5 knockdown also inhibited the viability, migration and invasion of MDA-MB231 cells, decreased the expression of p-STAT3, p-AKT, MMP9 and E2F1, and increased the expression of p21 in MDA-MB231 cells compared with cells stimulated with TGF-β1 alone. Therefore, GCN5 may work downstream of TGF-β/Smad signaling pathway to regulate the EMT in breast cancer.
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