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. 2013 Feb 1;14(5):436–449. doi: 10.4161/cbt.23787

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Figure 3. Effect of AK3 and AK10 on other colon cancer cell lines and on Fas-mediated cell death. (A) TNF was titrated on to HCT116 cells in the presence or absence of 20 μM AK3 or AK10. Although these cells are more inherently sensitive to TNF, AK3 significantly increased caspase activity as measured by DEVD-AMC cleavage (ANOVA, Tukey’s post hoc, *p < 0.01). AK10 did not significantly increase caspase activation in this cell line. (B) The mouse colon cancer cell line AJ02-NM0 was treated with AK3 or AK10 in the presence or absence of murine TNF and analyzed for caspase activity. Both AK3 and AK10 increased caspase activity in the presence of TNF, but not in its absence (*p < 0.001). AK3 was significantly more effective than AK10 (ANOVA, *p < 0.001). (C) AK3 and AK10 accentuated caspase activation by Fas ligation. HT29 cells were treated with AK3 or AK10 alone or in combination with an anti-Fas antibody (10 μg/ml) and analyzed for caspase activation. Although HT29 cells are sensitive to Fas ligation, both AK3 and AK10 significantly enhanced caspase activation (ANOVA, *p < 0.001).