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[Gleevec induces apoptosis in K562 cells through activating caspase-3].
- Source :
-
Yao xue xue bao = Acta pharmaceutica Sinica [Yao Xue Xue Bao] 2014 Aug; Vol. 49 (8), pp. 1124-9. - Publication Year :
- 2014
-
Abstract
- The present study is to elucidate the mechanisms underlying Gleevec-induced apoptosis of chronic myeloid leukemia (CML) K562 cells in vitro. The apoptotic cell death and cell cycle distribution after Gleevec treatment and the effect of PDCD4 siRNA on Gleevec-induced apoptosis of K562 cells were analyzed by flow cytometry. The effect of Gleevec on p-Crkl, caspase-3, PARP and PDCD4 protein levels, and the knockdown efficacy of PDCD4 siRNA were detected by Western blotting. The results showed that Gleevec dramatically suppressed the phosphorylation level of Crkl in a dose-dependent manner and induced significant apoptosis and G0/G1 cell cycle arrest of K562 cells in time- and dose-dependent manners. In addition, Gleevec activated caspase-3 and its downstream substrates PARP, and the caspase pan inhibitor Z-VAD-FMK (50 micromol x L(-1)) markedly reduced Gleevec-induced apoptosis from 47.97% +/- 10.56% to 31.05% +/- 9.206% (P < 0.05). Moreover, Gleevec significantly increased the protein expression of programmed cell death 4 (PDCD4). PDCD4 knockdown by siRNA reduced Gleevec-induced apoptosis from 46.97% +/- 14.32% to 42.8% +/- 11.43%. In summary, Gleevec induced apoptosis in K562 cells via caspase-3 activation.
Details
- Language :
- Chinese
- ISSN :
- 0513-4870
- Volume :
- 49
- Issue :
- 8
- Database :
- MEDLINE
- Journal :
- Yao xue xue bao = Acta pharmaceutica Sinica
- Publication Type :
- Academic Journal
- Accession number :
- 25322553