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. 2016 Apr 22;7(21):31534–31549. doi: 10.18632/oncotarget.8925

Figure 3. Phenotypic characterization of MUC16-targeted Meso64-TR3.

Figure 3

A. OVCAR3 cells were challenged with a constant amount of Meso64-TR3 (80% specific cell death) and increasing concentrations of soluble mesothelin to study the impact of the mesothelin/MUC16 interaction of Meso64-TR3. B. OVCAR3 cells were challenged with a constant amount of Meso64-TR3 (90% specific cell death) and increasing concentrations of DR5-Fc to verify involvement of the extrinsic death pathway as a mechanism of Meso64-TR3-induced cell death. C. OVCAR3 cells were seeded in 6-well plates and treated for 4 hours with TR3, Meso64-TR3 and medium as control. The cell pellets were submitted to Western blot analysis to examine the expression and activation status of caspase-8. D. OVCAR3 cells were seeded in 96-well plates and treated with Meso64-TR3 for 2, 4, 6, 8 h and the activity of caspase-3, caspase-8 and caspase-9 were detected using Caspase-Glo reagent. E. OVCAR3 cells were treated with a constant amount of Meso64-TR3 (90% specific cell death) in the presence of Z-VAD-FMK, a pan-caspase inhibitor to block the extrinsic death pathway. Cells treated with DMSO were used as a control. Error bars, mean ± SD. Results are representatives of at least 2 independent experiments done in triplicates. NS, not significant; ****P < 0.0001.