Trichostatin A reverses epithelial‑mesenchymal transition and attenuates invasion and migration in MCF‑7 breast cancer cells
Xiaoxiong Wang, Shirong Chen, Taipeng Shen, Hao Lü, Xiao Dingqiong, Meng Zhao, Yutang Yao, Xiuli Li, Ge Zhang, Xing Zhou, Xiao Jiang, Zhuzhong Cheng
Abstract
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.