Effect of IκBα2NΔ4 on the resistance of K562 and HL-60/Bcr-Abl cells to TNF-α–induced apoptosis
| . | % apoptotic cells* . | |
|---|---|---|
| Control . | TNF-α† (100 ng/mL) . | |
| K562 | ||
| RtTA‡ | 2.8 ± 1.5 | 5.0 ± 1.0 |
| IκBα2NΔ4‡ | 4.1 ± 2.0 | 11.7 ± 2.11-153 |
| HL-60 | ||
| Bcr-Abl | 2.9 ± 1.6 | 6.3 ± 1.4 |
| Bcr-Abl/Iκbα2NΔ4 | 3.3 ± 1.2 | 31.2 ± 3.61-155 |
| . | % apoptotic cells* . | |
|---|---|---|
| Control . | TNF-α† (100 ng/mL) . | |
| K562 | ||
| RtTA‡ | 2.8 ± 1.5 | 5.0 ± 1.0 |
| IκBα2NΔ4‡ | 4.1 ± 2.0 | 11.7 ± 2.11-153 |
| HL-60 | ||
| Bcr-Abl | 2.9 ± 1.6 | 6.3 ± 1.4 |
| Bcr-Abl/Iκbα2NΔ4 | 3.3 ± 1.2 | 31.2 ± 3.61-155 |
Detected by annexin V staining followed by flow cytometry.
These cells were cotreated with 3 μg/mL cycloheximide (CHX).
Pretreated with 1 μg/mL doxycycline for 48 hours.
Value significantly different from those in K562/rtTA cells treated with TNF-α + CHX (P < .05).
Value significantly different from those in HL-60/Bcr-Abl cells treated with TNF-α + CHX (P < .01).