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. 2020 Jan 15;10:377. doi: 10.1038/s41598-019-57285-y

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© The Author(s) 2020

Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/.

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Blockade of epigenetic modifications restores E-cadherin expression and cellular sensitivity to chemotherapy in EMT memory. (A) A schematic diagram of the experimental design. (B) Pre-treatment of TSA and EPZ prevented E-cadherin downregulation upon the acute IL-1β exposure. (C) AZA treatment restored E-cadherin expression in EMT memory. (D) Epigenetic inhibitors did not alter E-cadherin expression in chronic EMT. (E) Apoptosis markers were evaluated in chronic EMT and EMT memory following the combination of AZA and chemotherapy agents. Quantification of E-cadherin expression was normalized to samples without IL-1β exposure. Epi I, epigenetic inhibitors. AZA, 5′-azacytidine-2′-deoxycytidine (decitabine), DNA methyltransferase inhibitor; TSA, pan HDAC inhibitor; EPZ, EPZ-6438, EZH2 inhibitor; BIX, BIX01294, G9a inhibitor; OG-L, OG-L002, LSD1 inhibitor. “p”, previously treated with IL-1β. “n.d.”, non-detectable. See also Fig. S6.

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