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. 2017 Jun 27;7:4292. doi: 10.1038/s41598-017-04612-w

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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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ACF inhibits GSC growth in a dose-dependent fashion, and its anti-growth effect is augmented by hypoxia or by expression of, double-mutant, oxygen stable, forms of HIF-1α or HIF-2α. Growth curves of HSR-GBM1 (A,B), HSR040622 (B,C), and HSR040821 (E,F) treated with 0 (DMSO), 1, 5, 10, and 25 μM ACF in normoxia (21% oxygen; A,C,E) and hypoxia (1% oxygen; B,D,F). (G,H) Growth curve for HSR-GBM1 GSCs expressing GFP (as control) or the oxygen stable, double mutant (DM), forms of HIF-1α or HIF-2α, and treated with ACF at 0 (DMSO), 1 μM or 5 μM significantly reduced cell growth over a four-day period in normoxia. (H) A bar-graph analysis of day 4 time point is shown in (G). (***p < 0.001, **p < 0.01; One way ANOVA with multiple comparisons; Mean +/− SEM of triplicates is shown in all analyses).