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. 2016 Sep 6;115(8):929–939. doi: 10.1038/bjc.2016.278

Figure 1.

Figure 1

Vorinostat-mediated changes in histone acetylation, survival fraction and cell cycle distribution. (A) Western blots of acetylated histone H3 (AcH3) and total histone H3 under normoxia and following combinations of vorinostat (1 μM, 24 h) and hypoxia exposure (0.2% O2, 24 h) in DU 145, PC-3 and 22Rv1 prostate cancer cell lines. TUBG1 was included as loading control. H=hypoxia; N=normoxia. (B) Survival fraction under normoxia and following combinations of vorinostat (1 μM, 24 h) and hypoxia exposure (0.2% O2, 24 h) in DU 145, PC-3 and 22Rv1 prostate cancer cell lines. The data for combinations of vorinostat and hypoxia exposure were normalised to the survival fraction under normoxia. (C) Fraction of cells in different cell cycle phases under normoxia and following combinations of vorinostat (1 μM, 24 h) and hypoxia exposure (0.2% O2, 24 h) in DU 145, PC-3 and 22Rv1 prostate cancer cell lines. (B and C) Columns represent mean values from three independent experiments, and bars depict s.e.m. *Statistically significant difference.