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. 2020 Jul 29;20(4):2923–2940. doi: 10.3892/etm.2020.9073

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Copyright: © Xia et al.

This is an open access article distributed under the terms of the Creative Commons Attribution-NonCommercial-NoDerivs License, which permits use and distribution in any medium, provided the original work is properly cited, the use is non-commercial and no modifications or adaptations are made.

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Acetylation and deacetylation associated with EMT. Snail, a zinc finger protein, comprises a C-terminal zinc finger domain and an N-terminal SNAG domain. The C-terminal zinc finger domain recognizes the E-box sequence in the promoter region of E-cadherin. The SNAG domain associates with HDAC1/2 and corepressor mSin3A, and then recruits the repressor complex to the E-cadherin promoter, where HDAC1/2 deacetylate histone H3 and H4, inhibiting the expression of E-cadherin and promoting the process of EMT. Human c-Jun is a transcriptional regulator of JUN proto-oncogene. It is reported that the downregulation of HDAC3 expression can increase the acetylation of c-Jun and may lead to the degradation of c-Jun, which ultimately increases the expression of E-cadherin and decreases the expression of snail, thus inhibiting the process of EMT. EMT, epithelial-mesenchymal transition; Snail, zinc finger protein SNAI1; HDAC, histone deacetylase.