- Author:
Shu-Min DING
1
;
Rui-Rong XU
2
;
Jin-Yao KAN
3
;
Yan WANG
4
Author Information
- Publication Type:Journal Article
- MeSH: Antineoplastic Agents; Apoptosis; Arsenic Trioxide; Arsenicals; Cdc20 Proteins; HL-60 Cells; Humans; Leukemia, Myeloid, Acute; Oxides
- From: Journal of Experimental Hematology 2018;26(3):710-715
- CountryChina
- Language:Chinese
-
Abstract:
OBJECTIVETo investigate the effects of arsenic trioxide (AsO) on Cdc20 and Mad2 in process of AML HL-60 cell proliferation.
METHODSThe proliferation of HL-60 cells was detected by CCK-8 method at different concentrations of arsenic trioxide for 24, 48 and 72 hours. The cell morphological changes were observed by inverted microscopy. The expressions of Mad2 and Cdc20 mRNA and protein in HL-60 cells treated with AsO for 48 h were detected by real-time PCR and Western blot respectively.
RESULTSArsenic trioxide significantly inhibited the HL-60 cell proliferation and displayed a good time-dose correlation. RT-PCR and Western blot showed that the expression of Mad2 was up-regulated and the expression of Cdc20 was down-regulated in HL-60 cells treated with arsenic trioxide of different concentration (4,8,10 µmol/L).
CONCLUSIONArsenic trioxide can inhibit the human acute myeloid leukemia HL-60 cell proliferation, and its mechanism may be related with up-regulation of Mad2 expression and down-regulation of Cdc20 expression.