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. 2021 Nov 16;40:364. doi: 10.1186/s13046-021-02154-8

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© The Author(s) 2021, corrected publication 2022

Open AccessThis 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 licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence 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 licence, visit http://creativecommons.org/licenses/by/4.0/. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated in a credit line to the data.

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Fig. 6 — Effect of TAE226 > SOR on H3K27me3. A H3K27me3 levels measured by AlphaLISA assay and represented as fold change in HepG2 and Huh7 cells treated vs. NT. Data were analysed by 2-tailed Student’s t test. **p < 0.01; ***p < 0.001 vs. NT. Representative immunoblot (B) and quantitative analysis (C) of EZH2 expression after treatments, in HepG2 and Huh7 cells. αTubulin served as loading control. Values are the mean of arbitrary units ± SD of at least three independent experiments. Data were analysed by 2-tailed Student’s t test. *p < 0.05; **p < 0.01; ***p < 0.001 vs. NT