Celastrol down-regulates expression of P-Akt and cyclin D1 in HL-60 cells and induces apoptosis.
- Author:
Yong-Lan MA
1
;
Hong YI
;
Fei-Lan YANG
;
Yuan ZHANG
;
Ya WANG
;
Ying WANG
Author Information
1. Department of Clinical Laboratorial Examination, Air Force 457 Hospital of PLA, Wuhan 430012, Hubei Province, China.
- Publication Type:Journal Article
- MeSH:
Apoptosis;
drug effects;
Cyclin D1;
metabolism;
Down-Regulation;
Gene Expression Regulation, Leukemic;
HL-60 Cells;
Humans;
Proto-Oncogene Proteins c-akt;
metabolism;
Triterpenes;
pharmacology
- From:
Journal of Experimental Hematology
2010;18(4):898-902
- CountryChina
- Language:Chinese
-
Abstract:
The aim of this study was to investigate the effect of Celastrol on induction of HL-60 cell apoptosis and its possible mechanism. The proliferative activity of HL-60 cells treated with 0.25 - 8.0 μmol/L of Celastrol for 24 - 72 hours was assayed by MTT method, the effects of Celastrol on apoptosis and cell cycle of HL-60 were detected by TUNEL staining and flow cytometry with Annexin V-FITC/PI double labeling, the expression of pAkt and cyclin D1 at protein and gene level in HL-60 cells treated with Celastrol were measured by Western blot and RT-PCR. The results showed that the Celastrol could obviously inhibit the proliferation of HL-60 cells in concentration-and time-dependent manners, the IC₅₀ value of Celastrol for 24 hours was 6.21 ± 0.242 μmol/L. The Celastrol concentration-dependently induced the apoptosis of HL-60 cells, accompanying with morphological changes of apoptotic cells, which may be related with arrest of cells in G₀/G₁ phase. The Celastrol suppressed the expression of pAkt and Cyclin D1 in HL-60 cells to a varying degree which showed obvious concentration-and time-dependent manners. It is concluded that the Celastrol inhibits the proliferation and induced the apoptosis of HL-60 cells. Its mechanism may be related with down-regulation of p-Act and cyclin D1 expressions.
