SNAI1 interacts with HDAC1 to control TGF‑β2‑induced epithelial‑mesenchymal transition in human lens epithelial cells.

Abstract

The opacity of the lens capsule after cataract surgery is caused by epithelial‑to‑mesenchymal transition (EMT) of lens epithelial cells. Snail family transcriptional repressor 1 (SNAI1) is a transcriptional repressor that recruits multiple chromatin enzymes including lysine‑specific histone demethylase 1A, histone deacetylase (HDAC) 1/2, polycomb repressive complex2, euchromatic histone lysine methyltransferase 2 and suppressor of variegation 3‑9 homolog 1 to the E‑cadherin promoter, thereby suppressing E‑cadherin expression. However, the functional relationship between SNAI1 and HDAC in the induction of EMT in human lens epithelial cells (HLECs) is still unclear. Therefore, the objective of the present study was to explore the possible functional relationship between SNAI1 and HDAC1 in the induction of EMT in HLECs. In the present study, SNAI1 was found to be increased in HLECs during transforming growth factor‑β2 (TGF‑β2)‑induced EMT. Knockdown of SNAI1 by siRNA reversed TGF‑β2‑induced downregulation of E‑cadherin and upregulation of α‑Smooth Muscle Actin. Furthermore, SNAI1 was found to be associated with HDAC1 in the E‑cadherin promoter in TGF‑β2‑treated HLECs. Inhibition of HDAC by trichostatin A and suberoylanilide hydroxamic acid could prevent TGF‑β2‑induced EMT in HLECs. Collectively, SNAI1 interacted with HDAC1 to repress E‑cadherin in the TGF‑β2‑induced EMT in HLECs, suggesting that HDAC inhibitors may have potential therapeutic value for the prevention of EMT in HLECs.