Mechanism of antitumor effect of ursolic acid on T (8;21) leukemia cell kasumi-1.
10.7534/j.issn.1009-2137.2014.03.021
- Author:
Jun-Feng ZHANG
1
;
Li GAO
1
;
Hao-Qing DUAN
2
;
Wei WANG
1
;
Yan LI
1
;
Yi-Gai MA
3
Author Information
1. Department of Hematology, China-Japanese Friendship Hospital, Beijing 100029, China.
2. Department of Clinical Laboratorial Examination, Chinese PLA General Hospital, Beijing 100853, China.
3. Department of Hematology, China-Japanese Friendship Hospital, Beijing 100029, China. E-mail:dr_myg@yahoo.com.cn.
- Publication Type:Journal Article
- MeSH:
Apoptosis;
drug effects;
Cell Line, Tumor;
Cell Proliferation;
drug effects;
Humans;
Leukemia;
genetics;
Oncogene Proteins, Fusion;
genetics;
Translocation, Genetic;
Triterpenes;
pharmacology
- From:
Journal of Experimental Hematology
2014;22(3):687-691
- CountryChina
- Language:Chinese
-
Abstract:
This study was purposed to investigate the anti-tumor effect of ursolic acid (UA) on t(8;21) leukemia cell line kasumi-1 and its possible mechanisms. The kasumi-1 cells were treated with UA at different concentration for different duration of time. The growth inhibition of kasumi-1 treated with UA was detected by using CCK-8 test, and the morphological changes of kasumi-1 cells were observed by Wright's staining. Furthermore, the apoptosis rate of kasumi-1 was examined by flow cytometry. Lastly, the expression of AML1-ETO, KIT, MYC, CCND1, BCL-2, P53, BAX, MDM2 and protein were detected by using real-time quantitative PCR and Western blot respectively. The results showed that the UA obviously inhibited the growth of kasumi-1 cells in dose- and time-dependent manners. The apoptotic morphological changes of cells were presented when kasumi-1 cells were treated with UA for 48 hours. The apoptotic rate of kasumi-1 cells increased in a dose- and time-dependent ways, and the mRNA levels of AML1-ETO, KIT, MYC, CCND1, BCL2, MDM2 decreased in kasumi-1 cells treated with UA, as well as the protein levels. Meanwhile, UA up-regulated the mRNA and protein levels of P53 in the same manner. It is concluded that UA can exert its anti-tumor effect by inhibiting the proliferation and inducing the apoptosis of kasumi-1 cells in a dose-and time-dependent manners, that may provide the clues for a new targeting therapy to t(8;21) leukemia.
