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. 2017 Sep 7;7:10814. doi: 10.1038/s41598-017-11445-0

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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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Effects of HAT inhibitors on HIF-1α and ASS1 expression on cell killing by ADI and schematic diagram of epigenetic regulation of HIF-1a degradation. (a) Effects of PU139 on HIF-1α and ASS1 expression in the presence and absence of ADI. A2058 cells were treated with PU139 at the concentrations as indicated for 48 hr followed by treatment with or without ADI (0.5 μg/ml, 60 min). (b) Inhibition of ADI (0.5 μg/ml, 1 hr)-induced H3K27ac and H3K14ac deacetylation by PU139 (60 μM, 1 hr). (c) Similar experiment to that described in (A) except I-CBP112 was used. (d) Experiment similar to that described in (b) except I-CBP112 (20 μM for 1 hr) was used. (e, f) Effects on cell growth of PU 139 (20 μM for 48 hr) and I-CBP112 (30 μM, 48 hr) alone or together with ADI (0.5 μg/ml, 48 hr) by MTT assay as indicated. “ _*”, significant (P < 0.05, student’s t-test, n = 6). (g,h) Experiments similar to those described in (e) and (f), respectively, except using DNA fragmentation assay for apoptosis.