Effect of Dehydrocostus Lactone on Proliferation of K562 Cells and Its Mechanism.
10.19746/j.cnki.issn.1009-2137.2019.05.013
- Author:
Hong CAI
1
;
Chun-Hui YANG
2
;
Xiao-Lin HE
3
Author Information
1. Department of Clinical Laboratorial Examination, The Second Affiliated Hospital of Dalian Medical University, Dalian 116023, Liaoning Province, China.
2. Department of Clinical Laboratorial Examination, The Second Affiliated Hospital of Dalian Medical University, Dalian 116023, Liaoning Province, China,E-mail: yangchunhui627@163.com.
3. Department of Clinical Laboratorial Examination, The Second Affiliated Hospital of Dalian Medical University, Dalian 116023, Liaoning Province, China,E-mail: 17709875380@163.com.
- Publication Type:Journal Article
- MeSH:
Apoptosis;
Cell Proliferation;
Fusion Proteins, bcr-abl;
Humans;
K562 Cells;
Lactones;
Sesquiterpenes
- From:
Journal of Experimental Hematology
2019;27(5):1436-1439
- CountryChina
- Language:Chinese
-
Abstract:
OBJECTIVE:To explore the inhibitory effect of dehydrocostus lactone on the proliferation of human chronic myeloid leukemia K562 cells and the underlying mechanisms.
METHODS:Cell viability was evaluated by CCK-8 assay. Flow cytometry was used to assess the effect of dehydrocostus lactone on the cell cycle and apoptosis of K562 cells. The levels of BCR/ABL-STATs-related molecules were analyzed by using Western blot.
RESULTS:The CCK-8 assay showed that dehydrocostus lactone at graded concentration of 4, 6, 8, 10, 12 μmol/L could significantly inhibit the proliferation of K562 cells after exposure for 24 h. The proliferation inhibition rate was (24.32±3.05%), (42.91±3.89%), (46.35±4.93%), (77.06±5.42%) and (89.04±4.25%) respectively, showing statistically significantly different from (2.08±0.27%) in the control (P＜0.05). Also, the treatment with 5 and 10 μmol/L of dehydrocostus lactone induced K562 cell apoptosis, the apoptotic rate of K562 cells was significantly higher than that the control group (P＜0.05), and up-regulated the expression level of BAX and p21. Furthermore, dehydrocostus lactone (5 and 10 μmol/L) also increased the percentage of cells in G2/M [(8.53±1.71)% to (17.42±2.72) and (31.79±4.38%)](P＜0.05). The study results also revealed that dehydrocostus lactone significantly inhibited the expression of BCR/ABL STAT3, STAT5, CyclinB1, CDK1 and BCL-2, and up-regulated the expression level of BAX and p21.
CONCLUSION:Dehydrocostus lactone can suppress the proliferation of K562 cells and induce the apoptosis of K562 cells through BCR/ABL-STAT signaling pathways.
