Analysis of in vitro anti-leukemia effect of 5-aza-2'-deoxycitydine.
- Author:
Yan-hua XIAO
1
;
Hong YI
;
Tan TAN
;
Ting LIANG
;
Zhu-chu CHEN
;
Zhi-qiang XIAO
Author Information
1. Key Laboratory of Cancer Proteomics of Chinese Ministry of Health, Xiangya Hospital, Central South University, Changsha, China.
- Publication Type:Journal Article
- MeSH:
Antimetabolites, Antineoplastic;
pharmacology;
Apoptosis;
drug effects;
Azacitidine;
analogs & derivatives;
pharmacology;
Calgranulin A;
biosynthesis;
genetics;
Calgranulin B;
biosynthesis;
genetics;
Cell Proliferation;
drug effects;
Cell Transformation, Neoplastic;
drug effects;
Decitabine;
HL-60 Cells;
Humans;
RNA, Messenger;
biosynthesis;
genetics
- From:
Journal of Central South University(Medical Sciences)
2008;33(4):344-352
- CountryChina
- Language:Chinese
-
Abstract:
OBJECTIVE:To investigate the effect of methylation transferase inhibitor 5-aza-2'-deoxycitydine (5-aza-2 dC) on the growth, differentiation and apoptosis of human acute myeloid leukemia(AML) cell line HL-60, and to explore the possible anti-leukemia mechanism of 5-aza-2 dC.
METHODS:HL-60 cells were treated by 5-aza-2 dC at various concentrations for different periods of time. The effect of 5-aza-2 dC on the growth of HL-60 cells were detected by MTT assay. The effect on the cell cycle and differentiation were detected by flow cytometry. The effect on the apoptosis were detected by Hochest33342 staining and flow cytometry. The expression of S100A8 and S100A9 was detected by reverse transcription-polymerase chain reaction (RT-PCR).
RESULTS:(1) 5-aza-2 dC inhibited the growth of HL-60 cells in a concentration- and time-dependent manner, and HL-60 cells were arrested at G2/M phases; (2) 5-aza-2 dC enhanced the expression of cell differentiation antigen CD11b at HL-60 cells, especially at the low drug concentration; (3) 5-aza-2 dC induced HL-60 cell apoptosis in a concentration- and time-dependent manner, especially at the high drug concentration; (4) 5-aza-2 dC increased the expression levels of S100A8 and S100A9 mRNA in HL-60 cells.
CONCLUSION:5-aza-2 dC can inhibit the growth of HL-60 cells accompanied with G2/M phase arrest, induce the differentiation and apoptosis of the cells, and increase the expression levels of S100A8 and S100A9 mRNA, which may be the anti-AML mechanism of 5-aza-2 dC.
