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Article

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

  • Authors:
    • Ning Gao
    • Jingming Li
    • Yazhou Qin
    • Yingna Wang
    • Qianyang Kang
    • Cheng Pei
  • View Affiliations / Copyright

    Affiliations: Department of Ophthalmology, First Affiliated Hospital of Xi'an Jiaotong University, Xi'an, Shaanxi 710061, P.R. China
  • Pages: 265-273
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    Published online on: November 13, 2019
       https://doi.org/10.3892/ijmm.2019.4405
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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 complex 2, 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.
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Copy and paste a formatted citation
Spandidos Publications style
Gao N, Li J, Qin Y, Wang Y, Kang Q and Pei C: SNAI1 interacts with HDAC1 to control TGF‑β2‑induced epithelial‑mesenchymal transition in human lens epithelial cells. Int J Mol Med 45: 265-273, 2020.
APA
Gao, N., Li, J., Qin, Y., Wang, Y., Kang, Q., & Pei, C. (2020). SNAI1 interacts with HDAC1 to control TGF‑β2‑induced epithelial‑mesenchymal transition in human lens epithelial cells. International Journal of Molecular Medicine, 45, 265-273. https://doi.org/10.3892/ijmm.2019.4405
MLA
Gao, N., Li, J., Qin, Y., Wang, Y., Kang, Q., Pei, C."SNAI1 interacts with HDAC1 to control TGF‑β2‑induced epithelial‑mesenchymal transition in human lens epithelial cells". International Journal of Molecular Medicine 45.1 (2020): 265-273.
Chicago
Gao, N., Li, J., Qin, Y., Wang, Y., Kang, Q., Pei, C."SNAI1 interacts with HDAC1 to control TGF‑β2‑induced epithelial‑mesenchymal transition in human lens epithelial cells". International Journal of Molecular Medicine 45, no. 1 (2020): 265-273. https://doi.org/10.3892/ijmm.2019.4405
Copy and paste a formatted citation
x
Spandidos Publications style
Gao N, Li J, Qin Y, Wang Y, Kang Q and Pei C: SNAI1 interacts with HDAC1 to control TGF‑β2‑induced epithelial‑mesenchymal transition in human lens epithelial cells. Int J Mol Med 45: 265-273, 2020.
APA
Gao, N., Li, J., Qin, Y., Wang, Y., Kang, Q., & Pei, C. (2020). SNAI1 interacts with HDAC1 to control TGF‑β2‑induced epithelial‑mesenchymal transition in human lens epithelial cells. International Journal of Molecular Medicine, 45, 265-273. https://doi.org/10.3892/ijmm.2019.4405
MLA
Gao, N., Li, J., Qin, Y., Wang, Y., Kang, Q., Pei, C."SNAI1 interacts with HDAC1 to control TGF‑β2‑induced epithelial‑mesenchymal transition in human lens epithelial cells". International Journal of Molecular Medicine 45.1 (2020): 265-273.
Chicago
Gao, N., Li, J., Qin, Y., Wang, Y., Kang, Q., Pei, C."SNAI1 interacts with HDAC1 to control TGF‑β2‑induced epithelial‑mesenchymal transition in human lens epithelial cells". International Journal of Molecular Medicine 45, no. 1 (2020): 265-273. https://doi.org/10.3892/ijmm.2019.4405
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