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. 2015 Sep 11;7(1):97. doi: 10.1186/s13148-015-0131-z

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© Qin et al. 2015

Open AccessThis article is distributed under the terms of the Creative Commons Attribution 4.0 International License (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided 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 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.

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Fig. 7 — Carboplatin inhibits HP1α in the YB5 Cells. a. Effects of drug treatment on the expression of HP1 proteins. We isolated cytosolic and nuclear proteins and performed Western blot analysis of HP1α, HP1β, and HP1γ (* marks a non-specific band). Lamin B1 was used as the internal control for nuclear protein expression. β-actin was used as a control for both nuclear and cytosolic proteins. b. Expression of HP1α (CDX5) mRNA after drug treatment measured by real-time PCR and normalized to GAPDH. Statistical significance of gene expression changes was analyzed by one-way ANOVA (P = 0.005), and Tukey’s multiple comparison tests were used to analyzed the effects of the drug treatments compared to control (**P < 0.01). c. siRNA knockdown of HP1α increased expression of genes hypermethylated in the YB5 cells. The expression levels from four experiments were normalized to GAPDH and compared using t test (*P < 0.05). d. Knockdown of HP1α had little effect on genes with unmethylated promoters (P > 0.05)