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Journal of Experimental Hematology ; (6): 277-280, 2009.
Article in Chinese | WPRIM | ID: wpr-302149

ABSTRACT

This study was aimed to investigate the role of mitochondria pathway in signal transduction of chronic myeloid leukemia (CML). After bcr3/abl2 antisense oligodeoxynucleotide (ASO) was introduced into CML cell line K562 cells by liposomal transfection, the cell viability was detected by MTT assay, the cell apoptosis was determined by flow cytometry (FCM), the mitochondrial membrane potential (DeltaPsi) was labeled by Rhodamine 123 and examined by FCM, and the expression of mitochondrial apoptosis signal transduction pathway related proteins cytochrome C was analyzed by Western blot. The results showed that after K562 cells were exposed to 2 micromol/L of bcr3/abl2 ASO for 24 hours, bcr3/abl2 ASO significantly inhibited cell viability with inhibitory rate of 65.7%, induced the apoptosis of K562 cell line with apoptotic rate of 16.9%, and decreased mitochondrial Deltapsi of K562 cells with the reducing rate of 38.33%, enhanced the expression of cytochrome C with increase of optical density value from 2.33 +/- 0.3 to 4.78 +/- 0.1 by laser photometric scanning. It is concluded that mitochondria pathway plays an important role in signal transduction of chronic myeloid leukemia by directing apoptotic signal transduction.


Subject(s)
Humans , Apoptosis , K562 Cells , Leukemia, Myelogenous, Chronic, BCR-ABL Positive , Metabolism , Membrane Potential, Mitochondrial , Membrane Potentials , Mitochondria , Metabolism , Oligonucleotides, Antisense , Signal Transduction
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