DADS induces G2/M arrest through Chk1/Cdc25C/CyclinB1/CDK1 pathway in human leukemia HL-60 cells
10.3969/j.issn.1001-1978.2015.02.015
- VernacularTitle:DADS通过Chk1/Cdc25 C/CyclinB1/CDK1通路诱导白血病HL-60细胞G2/M期阻滞
- Author:
Xiaoxia JI
;
Ying ZENG
;
Jie HE
;
Hui TAN
;
Lan YI
;
Weiguo HUANG
;
Youhua WU
;
Qi SU
- Publication Type:Journal Article
- Keywords:
diallyl disulfide;
leukemia HL-60 cells;
growth inhibition;
G2/M arrest;
Chk1/Cdc25C/Cy-clinB1/CDK1 pathway;
molecular mechanism
- From:
Chinese Pharmacological Bulletin
2015;(2):221-226
- CountryChina
- Language:Chinese
-
Abstract:
Aim To study the effects of cycle arrest and molecular mechanism in human leukemia HL-60 cells induced by diallyl disulfide ( DADS ) . Methods Cell count, colony formation in soft agar experiments and flow cytometry analysis were employed to observe the DADS-induced cell growth inhibition and the effect of cycle arrest in HL-60 cells. The expressions of Chk1/2 and its downstream element in HL-60 cells were detected by Western blot. Results Cell count revealed that population doubling time increased to 35. 03 h and 71. 82 h, respectively, from 19. 14 h in HL-60 cells treated with 60 and 120 μmol·L-1 DADS ( P<0. 05 ) . Colony formation in soft agar experiments showed that colony formation inhibition rate of HL-60 cells exposed to 30, 60, 90 and 120μmol·L-1 DADS increased to 35. 06%, 62. 10%, 93. 79% and 99. 35%, respectively ( P<0. 05 ) . Flow cytometry a-nalysis exhibited that HL-60 cells treated with 60 and 120 μmol · L-1 DADS for 24 h and 48 h arrested in G2/M phase in a concentration-and time-dependent manner ( P <0. 05 ) . Western blot disclosed that the expression of p-Chk1 increased in a time-dependent manner ( P <0. 05 ); however, Chk1, Chk2 and p-Chk2 were not changed in HL-60 cells treated with 60μmol·L-1 DADS (P >0. 05). The expression of Cdc25C, CyclinB1 and CDK1 decreased after treated with 60 μmol·L-1 DADS in a time-dependent manner ( P<0. 05 ) , but the expression of 14-3-3 protein did not change ( P>0. 05 ) . Conclusion DADS can in-hibit the proliferation of HL-60 cells, and induce G2/M arrest through Chk1/Cdc25 C/CyclinB1/CDK1 path-way.
