Influence of Qingdai compound on expression of bcr/abl and JWA in K562 cells.
- Author:
Hai-Ping DAI
1
;
Qun SHEN
;
Jian-Wei ZHOU
;
Wei-Yan TANG
;
Guang-Rong ZHU
;
Wen XIA
Author Information
1. Department of Hematology, The Jiangsu TCM Hospital, Nanjing TCM University, Nanjing 210029, China.
- Publication Type:Journal Article
- MeSH:
Antineoplastic Agents, Phytogenic;
pharmacology;
Apoptosis;
drug effects;
Cell Proliferation;
drug effects;
Dose-Response Relationship, Drug;
Drugs, Chinese Herbal;
pharmacology;
Fusion Proteins, bcr-abl;
genetics;
Gene Expression Regulation, Neoplastic;
drug effects;
Heat-Shock Proteins;
genetics;
Humans;
Intracellular Signaling Peptides and Proteins;
genetics;
K562 Cells;
RNA, Messenger;
biosynthesis;
genetics;
Reverse Transcriptase Polymerase Chain Reaction
- From:
Journal of Experimental Hematology
2005;13(5):809-811
- CountryChina
- Language:Chinese
-
Abstract:
To study the effects of Qingdai compound on proliferation and apoptosis of K562 cells, as well as the expression of bcr/abl and JWA mRNA, K562 cells were treated in culture with different concentrations of Qingdai compound (2.5, 5, 7.5, 10 and 20 mg/ml) and harvested at 24 hours. Then morphological changes were observed by light microscopy (LM); expressions of bcr/abl and JWA were detected with semi-quantitative RT-PCR. The results showed that morphological changes were observed as the increment of the Qingdai compound concentration. Inhibition effects on proliferation and apoptosis in K562 cells were seen. A concentration-dependent decreases were found in bcr-abl and JWA mRNA expression of K562 cells. Qingdai compound partially inhibited proliferation and induced apoptosis of K562 cells. Expressions of both bcr/abl and JWA, which took part in cell proliferation and apoptosis, were down-regulated in a dose dependent manner. In conclusion, Qingdai compound can partially inhibit the expressions of bcr/abl and JWA genes in K562 cells, and the clinical effect of Qingdai compound on CML may be associated with apoptosis of leukemic cells.