Trichostatin A reverses epithelial-mesenchymal transition and attenuates invasion and migration in MCF-7 breast cancer cells.

Breast cancer remains one of the leading causes of mortality in women, and epithelial-mesenchymal transition (EMT) serves an indispensable role in the invasion and migration of breast cancer cells. As a representative of classical histone deacetylase inhibitors (HDACIs), trichostatin A (TSA) has been demonstrated to reverse EMT in certain types of non-tumor cells and tumor cells. In the present study, the invasive and migratory abilities of MCF-7 cells were examined following treatment with TSA. TSA-induced changes in the expression of an epithelial biomarker epithelial cadherin (E-cadherin), a mesenchymal biomarker (vimentin), and a transcription factor [zinc finger protein SNAI2 (SLUG)] were also investigated. Transwell invasion and migration assays, and wound healing assays, revealed that the invasive and migratory abilities of MCF-7 cells were suppressed significantly upon treatment with TSA. Treatment with TSA led to an increased expression level of E-cadherin, and decreased expression of vimentin and, in MCF-7 cells. The overexpression of SLUG decreased the expression level of E-cadherin, but increased vimentin expression, and upon treatment with TSA, these effects were reversed. Additionally, SLUG knockdown also led to upregulation of E-cadherin expression, downregulation of vimentin expression, and suppression of the invasion and migration of MCF-7 cells. Taken together, these results suggest that TSA is able to reverse EMT via suppressing SLUG and attenuate the invasion and migration of MCF-7 cells in vitro, thereby providing a potential avenue for chemotherapeutic intervention in the treatment of breast cancer.