Mechanism of G2/M blockage triggered by activated-Chk1 in regulation of drug-resistance in K562/A02 cell line / 中国实验血液学杂志
Journal of Experimental Hematology
;
(6): 1105-1109, 2006.
Article
in Chinese
| WPRIM
| ID: wpr-282721
ABSTRACT
The study was purposed to investigate the effect of phosphorylated-chk1 on cell cycle and apoptosis of human erythroleukemic cell line K562 and K562/A02, and to explore the mechanism of chk1 in regulation of drug-resistance of leukemia cells. After treatment with adrimycin for six hours, the cell cycle distribution was detected by flow cytometry; the Chk1mRNA expression was detected by RT-PCR and the Chk1 phosphorylation level was detected by Western blot. Under the condition of down-regulation of Chk1mRNA expression in cells transfected with Chk1 short hairpin RNA, the cell apoptosis rates were detected by flow-cytometry following adrimycin. The results indicated that the proportion of K562/A02 cell line in G2/M phase was (54.12 +/- 0.57)% at 6 hours after drug treatment, significantly higher than that of K562 cell line (36.99 +/- 1.28)%. No evident difference of the Chk1mRNA expression was observed between K562 and K562/A02 cell lines, while elevated Chk1 phosphorylation following DNA damage induced by adriamycin was observed in the K562/A02 cell line (0.79 +/- 0.56), significantly higher than that in K562 cell line (0.27 +/- 1.47). The cell apoptosis rate of the Chk1 shRNA group in K562/A02 cell line was 3.84-fold of blank vector group, but that in K562 cell line was 1.30-fold of blank vector group. It is concluded that the increased chk1 activity that delay the progress of cell cycle are associated with cellular resistance to adrimycin in the K562/A02 cell line.
Full text:
Available
Index:
WPRIM (Western Pacific)
Main subject:
Pharmacology
/
Phosphorylation
/
Physiology
/
Protein Kinases
/
RNA, Messenger
/
Signal Transduction
/
Doxorubicin
/
G2 Phase
/
Apoptosis
/
Drug Resistance, Neoplasm
Limits:
Humans
Language:
Chinese
Journal:
Journal of Experimental Hematology
Year:
2006
Type:
Article
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