The mechanism of arsenic trioxide-inducing apoptosis of K562 cells.
- Author:
Xu-Hui ZHANG
1
;
Ri ZHANG
;
Zi-Ling ZHU
;
Wei WANG
Author Information
1. Jiangsu Institute of Hematology, The First Affiliated Hospital of Suzhou University, Suzhou, 215006 China.
- Publication Type:Journal Article
- MeSH:
Antineoplastic Agents;
pharmacology;
Apoptosis;
drug effects;
Arsenicals;
pharmacology;
Caspase 3;
Caspases;
metabolism;
Cell Cycle;
drug effects;
Cell Proliferation;
drug effects;
Cytochromes c;
analysis;
Fusion Proteins, bcr-abl;
genetics;
Humans;
K562 Cells;
Oxides;
pharmacology;
Proto-Oncogene Proteins c-bcl-2;
genetics;
bcl-X Protein
- From:
Journal of Experimental Hematology
2004;12(5):558-562
- CountryChina
- Language:Chinese
-
Abstract:
The aim was to investigate the mechanism of arsenic trioxide (ATO) inducing apoptosis of K562 cells that express P210Bcr-Abl. Apoptosis was analyzed by cell proliferation assay, morphological changes, DNA-PI staining and cell cycle analysis. ELISA kits were also used to analyze the concentration of cytosolic cytochrome C and activation of caspase-3. Transcriptional levels of Bcl-XL and Bcr-Abl were assayed by semiquantitative reverse transcription polymerase chain reaction (RT-PCR). The results showed that K562 cells were induced to apoptosis after exposure to 2.5 micromol/L ATO for at least 48 hours, and the cell cycle of K562 cells was arrested at the G2/M phase. Caspase-3 was activated and there was a cytosolic accumulation of cytochrome C. ATO could only reduce the transcriptional level of Bcl-XL, but could not down-regulate the Bcr-Abl transcriptional level. In conclusion, ATO can induce K562 cells to apoptosis. The signal pathway mediated by the cytosolic translocation of mitochondria cytochrome C is one of the mechanisms for ATO inducing apoptosis. And the decrease of Bcl-XL may induce more apoptosis.
