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. 2017 Jun 15;7:3568. doi: 10.1038/s41598-017-03362-z

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© The Author(s) 2017

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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Inhibition of EZH2 converts histone modification mark occupancy at the TIMP2 promoter. (a) Western blot analysis of different histone modification marks in A2780 and SKOV3 cells after EZH2 knockdown or pharmacological inhibition by GSK126 treatment (b). The cropped blots are used in the figure, and full-length blots are presented in Supplementary Figs S18 and S19. (c) ChIP analysis of different histone modification marks at the TIMP2 promoter in A2780 and SKOV3 cells. IgG served as a negative control. (d,e) ChIP analysis of different histone modification marks at the TIMP2 promoter in A2780 and SKOV3 cells treated by GSK126. (f,g) ChIP analysis of different histone modification marks in EZH2-knockdown A2780 and SKOV3 cells. The results were normalized to the input. The EZH2 target gene KLF2 was used as a positive control. *P < 0.05; **P < 0.01; ***P < 0.001. NS, not significant.