Results: 5

1.
Figure 1

Figure 1. From: Inhibition of Glutathione and Thioredoxin Metabolism Enhances Sensitivity to Perifosine in Head and Neck Cancer Cells.

Effect of perifosine (PER) on Akt expression. Akt phosphorylation in FaDu, Cal-27, and SCC-25 cells was assayed by Western blots (50 μg protein loaded in each well) for Akt and phosphor-Akt Ser473 in the presence or absence of 5 μM PER for 24 hours. GAPDH was used as a loading control.

Andrean L. Simons, et al. J Oncol. 2009;2009:519563.
2.
Figure 5

Figure 5. From: Inhibition of Glutathione and Thioredoxin Metabolism Enhances Sensitivity to Perifosine in Head and Neck Cancer Cells.

Association of perifosine-(PER-) induced cytotoxicity with glutathione (GSH) content and thioredoxin reductase activity (TrxRed) in head and neck cancer cells. FaDu, Cal-27, and SCC-25 cells were analyzed for mean baseline TrxRed activity (a) and mean total GSH content (b) and compared to their respective mean surviving fraction in response to 5 μM PER (FaDu and Cal-27) or 10 μM PER (SCC-25).

Andrean L. Simons, et al. J Oncol. 2009;2009:519563.
3.
Figure 2

Figure 2. From: Inhibition of Glutathione and Thioredoxin Metabolism Enhances Sensitivity to Perifosine in Head and Neck Cancer Cells.

Effect of perifosine (PER) in head and neck cancer cell growth and survival. FaDu (a), Cal-27 (b), and SCC-25 (c) cells were treated with 1, 5, and 10 μmol/L PER and grown for 72 hours. (d) Cells were treated with 1–10 μM PER for 24 hours then plated for clonogenic survival. Clonogenic cell survival data were normalized to control (CON). Error bars represent ± 1SD of N = 4–6 experiments performed on different days with at least 2 cloning dishes taken from 1 treatment dish. ∗, P < .05 versus control.

Andrean L. Simons, et al. J Oncol. 2009;2009:519563.
4.
Figure 3

Figure 3. From: Inhibition of Glutathione and Thioredoxin Metabolism Enhances Sensitivity to Perifosine in Head and Neck Cancer Cells.

Effect of perifosine (PER) and N-acetyl-cysteine (NAC) on total glutathione (GSH) levels (a), glutathione disulfide (GSSG) levels (b), percentage glutathione disulfide (%GSSG) levels (c), and cytotoxicity (d) in head and neck cancer cells. Cells were treated with 5 μM PER (FaDu and Cal-27) or 10 μM PER (SCC-25) for 24 hours with or without treatment with 20 mM NAC for 1 hour before and during PER exposure. (a)–(c) Cells were harvested for glutathione analysis using the spectrophotometric recycling assay. Error bars represent ± 1SD of N = 4 experiments. (d) Cells were analyzed for clonogenic survival and the data were normalized to control (CON). Error bars represent ± 1SD of N = 3 experiments performed on different days with at least 2 cloning dishes taken from 1 treatment dish. ∗, P < .001 versus control; ¥, P < .001 versus respective treatment without NAC.

Andrean L. Simons, et al. J Oncol. 2009;2009:519563.
5.
Figure 4

Figure 4. From: Inhibition of Glutathione and Thioredoxin Metabolism Enhances Sensitivity to Perifosine in Head and Neck Cancer Cells.

Effect of inhibitors of glutathione and thioredoxin metabolism on perifosine (PER) toxicity in head and neck cancer cells. (a) Cal-27 and SCC-25 cells were treated with 5 μM PER (Cal-27) or 10 μM PER (SCC-25) for 24 hours with or without treatment with 1 mM buthionine sulfoximine (BSO) for 1 hour before and during PER exposure. (b)-(c) Cells were treated as stated above and harvested for total glutathione (GSH) levels (b), and percentage glutathione disulfide (%GSSG) levels (c) using the spectrophotometric recycling assay. Error bars represent ± 1SD of N = 3 experiments. (d) Cal-27 and SCC-25 cells were treated with 5 μM PER (Cal-27) or 10 μM PER (SCC-25) for 24 hour with or without treatment with 0.5 μM Auranofin (AUR) for 1 hour before and during PER exposure. Clonogenic cell survival data were normalized to control (CON). Error bars represent ± 1SD of N = 3 experiments performed on different days with at least 4 cloning dishes taken from 1 treatment dish. ∗, P < .001 versus control; ¥, P < .05 versus respective treatment without BSO or AUR.

Andrean L. Simons, et al. J Oncol. 2009;2009:519563.

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