Effect of adriamycin on Gfi-1 expression in K562 cells and its relationship with the relevant apoptotic genes.
- Author:
Wei CHANG
1
;
Han-Ying SUN
;
Min HUANG
;
Jian-Feng ZHOU
;
Yi-Cheng ZHANG
Author Information
1. Department of Hematology, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan 430030, China.
- Publication Type:Journal Article
- MeSH:
Antibiotics, Antineoplastic;
pharmacology;
Apoptosis;
drug effects;
DNA-Binding Proteins;
biosynthesis;
genetics;
Doxorubicin;
pharmacology;
Humans;
K562 Cells;
Proto-Oncogene Proteins c-bcl-2;
metabolism;
RNA, Messenger;
biosynthesis;
genetics;
Transcription Factors;
biosynthesis;
genetics;
bcl-2-Associated X Protein;
metabolism
- From:
Journal of Experimental Hematology
2007;15(2):278-282
- CountryChina
- Language:Chinese
-
Abstract:
The study was purposed to explore the effect of adriamycin (ADM) on K562 cells in vitro and the mechanism of expression changes of relevant apoptotic genes and oncogene Gfi-1. The apoptosis was assayed by flow cytometry (FCM) and the DNA electrophoresis; the expression changes of Gfi-1, Bcl-2, bax mRNA and protein were detected by RT-PCR and FCM after K562 cells were treated with different concentrations of ADM for 24 hours. The results showed that when K562 cells were treated with 0 - 2.0 mg/L ADM for 24 hours, the typical apoptotic DNA electrophoresis band of K562 cells were observed with the dose increasing. When concentration of ADM was 0.5 and 2.0 mg/L, the expression of Gfi-1 decreased and the expression of bax increased; when concentration of ADM was 0.5 - 2.0 mg/L, the expression of Bcl-2 was not found to be significantly changed, the levels of Bcl-2 mRNA and protein were of no statistical difference. When dose of ADM was higher than 2.0 mg/L, the percentage of apoptotic K562 cells decreased with cell necrosis. It is concluded that at certain range of concentration, apoptosis or necrosis of K562 cells can be induced by ADM, the percentage of apoptosis, the changes of expression of Bcl-2, bax and Gfi-1 depend on the dose of ADM. The mechanism of apoptosis in K562 cells induced by ADM may be related to suppression of Gfi-1 oncogene and activation of expression of bax gene.
