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. 2017 Nov 3;25(2):340–352. doi: 10.1038/cdd.2017.164

Figure 2.

Figure 2

Caspase-8 activation is p53- and death receptor-independent. (a) HCT116 and HCTp53−/− (p53−/−) cells were treated with 5FU for 24, 48 and 72 h before apoptosis was measured. Data are plotted as mean±S.E.M. (n≥3). (b) Caspase-8 activity following 5FU treatment was measured in HCT116 and p53−/− cells. Data are plotted as mean±S.E.M. (n=4). (c) Caspase-8 was silenced in p53−/− cells (shC8) and apoptosis measured 72 h post-treatment. Control knockdown cells (shctrl.) were used for comparison. Data are plotted as mean±S.E.M. (n=3). (d) MMP measurements in HCT116 and p53−/− cells before (−) and after (+) 5FU treatment. Data are plotted as mean±S.E.M. (n=3). (e) Apoptosis and changes in MMP after 5FU treatment were measured in stable Bid-silenced HCT116 cells (shBid). Data are plotted as mean±S.E.M. (n=3). (f) Caspase-8 activity following 5FU treatment was measured in HCT.shBid cells. Data are plotted as mean±S.E.M. (n=4). (g) XIAP was silenced (Ad.shXIAP) in HCT.shctrl and HCT.shBid cells and apoptosis measured after 5FU treatment. Data are plotted as mean±S.E.M. (n=3). Controls were shEGFP (Ad.shEGFP) double knock-downs. (h) HCT116 cells were silenced for p53 and XIAP (Ad.shp53 and Ad.shXIAP) and apoptosis measured following 5FU treatment. Ad.shEGFP and Ad.shsc served as double knockdown control. Data are plotted as mean±S.E.M. (n≥3).