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. 2017 Jun 5;7:2798. doi: 10.1038/s41598-017-02935-2

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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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Downregulation of UHRF1 leads to upregulation of CXCR4 via epigenetic modulation. (a) qRT-PCR analysis for the mRNA expression level of CXCR4 in shCont- and shUHRF1-HepG2 cells. (b) ChIP analysis for the presence of UHRF1 on the CXCR4 promoter in shCont- or shUHRF1-HepG2 cells. Chromatin was immunoprecipitated with an anti-UHRF1 antibody. (c) ChIP analysis for the presence of p300 on the CXCR4 promoter in shCont- or shUHRF1-HepG2 cells. Chromatin was immunoprecipitated with an anti-p300 antibody. (d) ChIP analysis for the presence of H3K27ac and H3K9me on the CXCR4 promoter in shCont- or shUHRF1-HepG2 cells. Chromatin was immunoprecipitated with an anti-H3K27ac or -H3K9me antibody. The results show the percentage of the input chromatin (1%). IgG was used as the antibody control. Results from three independent experiments are expressed as means ± SEMs. (*P < 0.05, **P < 0.01).