Fig. 4.
Fig. 4. Blocking caspase 8 activation enhances HL60 cell survival by inhibiting downstream caspase 3 activation and cell death. (A) HL60 cells (1 × 106/mL) were incubated with C1 or C2 (100 μg/mL) in the presence or absence of IETD-CHO (50 μmol/L) for 18 hours and cell survival was determined by MTT assay. Data shown are the mean ± SD of three independent experiments. (B) C1-and C2-treated HL60 cells were assessed for apoptotic phenotype in the presence of IETD-CHO (50 μmol/L) by annexin V-FITC staining by flow cytometry as described in Materials and Methods. Data are shown as the percentage of annexin V positive. (C) Cell lysates obtained from HL60 cells (1 × 106) after exposure to 100 μg/mL of C1 or C2 for 12 hours in the presence or absence of IETD-CHO (50 μmol/L) were analyzed for caspase 3 activation (DEVDase activity). Data are shown as X increase in caspase 3 activity.

Blocking caspase 8 activation enhances HL60 cell survival by inhibiting downstream caspase 3 activation and cell death. (A) HL60 cells (1 × 106/mL) were incubated with C1 or C2 (100 μg/mL) in the presence or absence of IETD-CHO (50 μmol/L) for 18 hours and cell survival was determined by MTT assay. Data shown are the mean ± SD of three independent experiments. (B) C1-and C2-treated HL60 cells were assessed for apoptotic phenotype in the presence of IETD-CHO (50 μmol/L) by annexin V-FITC staining by flow cytometry as described in Materials and Methods. Data are shown as the percentage of annexin V positive. (C) Cell lysates obtained from HL60 cells (1 × 106) after exposure to 100 μg/mL of C1 or C2 for 12 hours in the presence or absence of IETD-CHO (50 μmol/L) were analyzed for caspase 3 activation (DEVDase activity). Data are shown as X increase in caspase 3 activity.

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