Triptolide inhibits proliferation and induces apoptosis of imatinib resistant K562/G01 cells.
10.7534/j.issn.1009-2137.2013.05.012
- Author:
Si-Qun WEN
1
;
Liang-Ming MA
;
Yu-Jin LU
;
Bo BAI
Author Information
1. Department of Hematology, Shangxi Big Hospital of Shangxi Medical University, Taiyuan 030032, Shangxi Province, China.
- Publication Type:Journal Article
- MeSH:
ATP Binding Cassette Transporter, Sub-Family B;
ATP-Binding Cassette, Sub-Family B, Member 1;
genetics;
Apoptosis;
drug effects;
Benzamides;
pharmacology;
Cell Cycle Checkpoints;
Cell Proliferation;
drug effects;
Diterpenes;
pharmacology;
Drug Resistance, Neoplasm;
Epoxy Compounds;
pharmacology;
Fusion Proteins, bcr-abl;
genetics;
Humans;
Imatinib Mesylate;
K562 Cells;
Phenanthrenes;
pharmacology;
Piperazines;
pharmacology;
Pyrimidines;
pharmacology
- From:
Journal of Experimental Hematology
2013;21(5):1148-1152
- CountryChina
- Language:Chinese
-
Abstract:
This study was aimed to explore the inhibitory effect of triptolide on proliferation and inducing apoptosis effect of K562/G01 cells and their possible mechanism. MTT assay was used to detect the effect of imatinib or triptolide alone and their combination on K562/G01 proliferation; the cell cycle, apoptosis rate, P-gp protein expression were detected by flow cytometry (FCM); the expression of P-gp was assessed by Western blot; the BCR/ABL gene expression was assayed by real time quantitative PCR. The results showed that triptolide could enhance the effect of imatinib on proliferation inhibition and apoptosis of K562/G01, arrested the cell cycle in G1 phase, down-regulated the expression of BCR/ABL gene and P-gp protein. It is concluded that triptolide induces K562/G01 cell proliferation inhibition and apoptosis, the mechanism may be related to cell cycle arrest, decrease of P-gp protein expression, inhibition of BCR/ABL gene expression.
