Alantolactone inhibits the proliferation of K562/ADR cells through regulating expression of cell cycle-related proteins
10.3760/cma.j.issn.1009-9921.2015.11.001
- VernacularTitle:土木香内酯通过调节细胞周期相关蛋白的表达抑制慢性粒细胞白血病耐药细胞株K562/ADR增殖
- Author:
Chunhui YANG
;
Hong CAI
;
Xiuxiang MENG
;
Tonghui MA
- Publication Type:Journal Article
- Keywords:
Alantolactone;
Leukemia;
Cell proliferation;
Cell cycle
- From:
Journal of Leukemia & Lymphoma
2015;24(11):641-644,661
- CountryChina
- Language:Chinese
-
Abstract:
Objective To investigate the effects of alantolactone on cell proliferation,cell-cycle and cell cycle-related proteins in human chronic myelogenous leukemia drug-resistant cell line K562/ADR.Methods K562/ADR cells were treated with 0,1.0,2.0,4.0,6.0,8.0,and 10.0 μmol/L of alantolactone for 12,24 and 48 h,with its cell viability analyzed by MTT assay.Flow cytometry was used to examine the effect of alantolactone on the cell-cycle of K562/ADR cells.The cell cycle-related proteins were analyzed by using Western blot after treatment with alantolactone.Results The results of MTT showed that alantolactone effectively inhibited the proliferation of K562/ADR cells in dose and time-dependent way,and the IC50 value of alantolactone in K562/ADR cells was about 5 μmol/L.Flow cytometric analysis displayed that alantolactone could arrest cell cycle at G2/M phase.The percentage of accumulated cells in the G2/M phase was increased from (15.8±1.7) ％ in the control group to (21.0±2.4) ％,(26.4±2.7) ％,and (30.1±3.9) ％ in cells treated with 2.5,5.0,and 7.5 μmol/L of alantolactone for 24 h,respectively (P ＜ 0.05).Alantolactone significantly decreased the expression of CDK1 and CyclinB1 and increased the expression of cyclin-dependent kinase inhibitor p21.Meanwhile,the treatment of K562/ADR with alantolactone led to a dose-dependent decrease in bcr-abl protein levels.Conclusion Alantolactone can significantly inhibit the proliferation and cell-cycle arrest in G2/M phase of K562/ADR cells,in which mechanism may be associated with the regulation of cell cycle-related proteins and downregulation of bcr-abl protein.
