Bcl-2-AS increases apoptosis induced by ara-C
| Samples . | Subdiploid apoptotic cells (%) . | Bcl-2 expression (×103 ABC per cell) . | ||||
|---|---|---|---|---|---|---|
| Control . | NS . | Bcl-2-AS . | Control . | NS . | Bcl-2-AS . | |
| Responsive blasts (N = 7) | ||||||
| No ara-C | 18.5 ± 5.6 | 26.9 ± 6.6 | 43.8 ± 8.1 | 23.7 ± 7.8 | 25.7 ± 5.4 | 16.7 ± 5.5 |
| Ara-C | 42.3 ± 5.8 | 42.6 ± 5.8 | 61.7 ± 7.0 | 30.4 ± 7.1 | 29.2 ± 8.1 | 13.5 ± 3.0 |
| Nonresponsive blasts (N = 6) | ||||||
| No ara-C | 20.5 ± 5.7 | 18.9 ± 5.4 | 20.5 ± 5.7 | 49.2 ± 9.9 | 53.0 ± 6.2 | 35.3 ± 6.7 |
| Ara-C | 46.4 ± 11.2 | 42.5 ± 11.0 | 42.3 ± 11.6 | 42.8 ± 5.8 | 44.6 ± 6.3 | 36.3 ± 4.5 |
| Samples . | Subdiploid apoptotic cells (%) . | Bcl-2 expression (×103 ABC per cell) . | ||||
|---|---|---|---|---|---|---|
| Control . | NS . | Bcl-2-AS . | Control . | NS . | Bcl-2-AS . | |
| Responsive blasts (N = 7) | ||||||
| No ara-C | 18.5 ± 5.6 | 26.9 ± 6.6 | 43.8 ± 8.1 | 23.7 ± 7.8 | 25.7 ± 5.4 | 16.7 ± 5.5 |
| Ara-C | 42.3 ± 5.8 | 42.6 ± 5.8 | 61.7 ± 7.0 | 30.4 ± 7.1 | 29.2 ± 8.1 | 13.5 ± 3.0 |
| Nonresponsive blasts (N = 6) | ||||||
| No ara-C | 20.5 ± 5.7 | 18.9 ± 5.4 | 20.5 ± 5.7 | 49.2 ± 9.9 | 53.0 ± 6.2 | 35.3 ± 6.7 |
| Ara-C | 46.4 ± 11.2 | 42.5 ± 11.0 | 42.3 ± 11.6 | 42.8 ± 5.8 | 44.6 ± 6.3 | 36.3 ± 4.5 |
Bcl-2-AS, Bcl-2 antisense oligodeoxynucleotides; ABC, antibody-binding capacity; NS, nonsense oligodeoxynucleotides.
The percentage of apoptotic cells was determined using flow cytometry of acridine orange staining as described in “Materials and methods.” The combination of Bcl-2-AS with 1 μmol/L ara-C significantly (P < .05) enhanced ara-C induced apoptosis in responsive blast samples but not in nonresponsive blast samples after 72 hours of treatment. The level of Bcl-2 expression in AML cells treated with Bcl-2-AS or NS did not change significantly when ara-C was added. All measurements of the Bcl-2 expression were analyzed after appropriate gating on live CD34+ AML cells.