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. 2014 Dec 8;3(12):e131. doi: 10.1038/oncsis.2014.47

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Copyright © 2014 Macmillan Publishers Limited

Oncogenesis is an open-access journal published by Nature Publishing Group. This work is licensed under a Creative Commons Attribution-NonCommercial-NoDerivs 4.0 International License. The images or other third party material in this article are included in the article's Creative Commons license, unless indicated otherwise in the credit line; if the material is not included under the Creative Commons license, users will need to obtain permission from the license holder to reproduce the material. To view a copy of this license, visit http://creativecommons.org/licenses/by-nc-nd/4.0/

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(a) Representative image of control (dimethyl sulfoxide (DMSO)) and sulforaphane-treated (12 h) PC3 cells with nuclear (4,6-diamidino-2-phenylindole (DAPI)) and SUV39H1 labeling for immunofluorescent imaging. The chromatin-associated SUV39H1 foci and dispersed nuclear and perinuclear mobile fractions are readily visible. (b) Sulforaphane leads to a decrease in chromatin-associated SUV39H1. PC3 cells were treated for 8 h with sulforaphane. MG132 was spiked into the culture dishes at a final concentration of 50 μM for the last 2 h of the treatment. The high-dose, short-duration treatment was to halt a sulforaphane-stimulated increase in proteasome activity and decrease the impact of any MG132 toxicity. The experimental conditions did inhibit protein degradation (increase in ubiquitinated proteins in sulforaphane-treated PC3 cells). (c) Densitometry showed a decrease in histone-associated SUV39H1 and an increase in mobile SUV39H1 (*P<0.05, **P<0.01 by two-way analysis of variance with Bonferroni post test, mean+s.d.). Histone-associated (nuclear, immobile) SUV39H1 normalized to nuclear marker fibrillarin. Mobile (cytoplasmic) SUV39H1 normalized to β-actin. SFN, sulforaphane.