The mechanism of STI571 inducing apoptosis of K562 cells.
- Author:
Yazhen QIN
1
;
Shanshan CHEN
;
Yan CHANG
;
Jiayu FU
;
Xinjuan WANG
Author Information
- Publication Type:Journal Article
- MeSH: Antineoplastic Agents; pharmacology; Apoptosis; Benzamides; Caspase 3; Caspases; metabolism; Cytochrome c Group; metabolism; Cytoplasm; metabolism; Enzyme Precursors; metabolism; Fusion Proteins, bcr-abl; metabolism; Humans; Imatinib Mesylate; K562 Cells; Membrane Potentials; drug effects; Mitochondria; drug effects; Piperazines; pharmacology; Pyrimidines; pharmacology; Reactive Oxygen Species; metabolism
- From: Chinese Journal of Hematology 2002;23(6):289-292
- CountryChina
- Language:English
-
Abstract:
OBJECTIVETo investigate the mechanism of STI571 inducing apoptosis of K562 cells which express P210(BCR/ABL).
METHODSApoptosis was analyzed by Annexin-V/PI, DioC6 [3] staining, DCFH-DA staining, DNA-PI staining and DNA ladder. Western blot was used to analyse mitochondrial and cytosolic cyto C, Bcl-X(L), caspase-3, actin protein and the level of tyrosine phosphorylation.
RESULTSAfter exposure to STI571, K562 cells were induced to apoptosis. Tyrosine phosphorylation level of P210(BCR/ABL) and Bcl-X(L) was decreased. Caspase-3 was activated and there was an cytosolic accumulation of cyto C.
CONCLUSIONSTI571 could rapidly decrease the tyrosine phosphorylation level of P210(BCR/ABL). The signal pathway mediated by the cytosolic translocation of mitochondrial cyto C was one of the mechanisms that STI571 inducing apoptosis. STI571 was an effective gene targeting therapeutic agent.
