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. Author manuscript; available in PMC: 2018 May 18.
Published in final edited form as: Clin Exp Metastasis. 2018 Feb 2;35(1-2):37–51. doi: 10.1007/s10585-018-9876-z

Fig. 1.

Fig. 1

P-AscH-induced cytotoxicity in hypoxia. a Treatment of MIA PaCa-2 cells with P-AscH (7 mM; 7 pmol cell−1) significantly increased doubling time (n = 6, *p < 0.05 vs. control). b P-AscH (10 mM; 10 pmol cell−1) significantly increased doubling time in PANC-1 cancer cell lines (n = 6, p < 0.05). c Clonogenic survival was decreased in a dose-dependent fashion in MIA-PaCa-2 cells treated and subsequently grown in 4% O2 (n = 3, *p < 0.01 vs. control). d Clonogenic survival was decreased in a dose-dependent fashion in PANC-1 cells treated and subsequently grown in 4% O2 (n = 3, *p < 0.01 vs. control). e Clonogenic survival was decreased in a dose-dependent fashion in 339 cells treated and subsequently grown in 4% O2 (n = 4, *p < 0.01 vs. control). f P-AscH-induced decreases in clonogenic survival were similar in hypoxic environments (7 pmol/cell, 7 mM P-AscH, means ± SEM, n = 3, *p < 0.05 vs. control). g Catalase reverses P-AscH-induced cytotoxicity in 1% O2 (7 pmol/cell, 7 mM P-AscH, means ± SEM, n = 3, *p < 0.05 vs. control). h Clonogenic survival of P-AscH treated cells pre-conditioned to hypoxia by 16-h incubation in 4% O2 compared to unconditioned cells and cells treated in 20% O2. Cells conditioned to hypoxia were significantly sensitive to P-AscH (7 pmol/cell, 7 mM P-AscH, n = 3, p < 0.01), however, pre-conditioning to hypoxia yielded no significant resistance to P-AscH relative to unconditioned controls, or cells treated in 20% O2