Effect of 5-aminoimidazole-4-formamide Ribonucleotide Combined with Interferon on Chronic Myeloid Leukemia K562 Cells.
10.19746/j.cnki.issn.1009-2137.2020.06.017
- Author:
Hong-Juan WANG
1
;
Rui LIU
2
;
Yuan-Yuan ZHANG
;
Fan-Mei GE
3
Author Information
1. Department of Hematology and Endocrinology, Xianyang Hospital of Yan'an University, Xianyang 712000, Shaanxi Province, China.
2. Department of Hematology and Endocrinology, Xianyang Hospital of Yan'an University, Xianyang 712000, Shaanxi Province, China,E-mail 644073252@qq.com.
3. Department of Hematology and Immunology, The Affiliated Hospital of Yan'an University, 716000 Yan'an, Shaanxi Province, China,E-mail: Gfmei@126.com.
- Publication Type:Journal Article
- MeSH:
Apoptosis;
Cell Proliferation;
Formamides;
Humans;
Imidazoles;
Interferons;
K562 Cells;
Leukemia, Myelogenous, Chronic, BCR-ABL Positive;
Ribonucleotides/pharmacology*
- From:
Journal of Experimental Hematology
2020;28(6):1892-1898
- CountryChina
- Language:Chinese
-
Abstract:
OBJECTIVE:To study the effect of 5-aminoimidazole-4-formamide ribonucleotide (AICAR) combined with interferon (IFN-α-2b) on the proliferation and apoptosis of chronic myeloid leukemia K562 cells, and explore its possible mechanism.
METHODS:CCK-8 method was used to detect the inhibition of cell proliferation. Wright Giemsa method was used to stain and cell morphology was observed by light microscopy. FITC Annexin V/PI double staining method was used to analyze the change of apoptosis rate. Immunocytochemistry method was used to detect the expression of wild-type P53 protein.
RESULTS:Different concentration of AICAR was inhibitory effect on K562 cells at different time point of action for 24 h, 48 h, and 72 h, and the inhibition was time and dose-dependent (r=0.71, r=0.84). The combination of AICAR and IFN-α-2b could effectively inhibit the proliferation and promote apoptosis of K562 cells. The inhibition rate of K562 cells was (45.26±2.54)%, and the early apoptosis rate was (33.72±0.23)%, which was statistically significantly different from the control group, AICAR or IFN-ɑ-2b alone (P<0.05). The combination of two drugs promoted the expression of wild-type p53 protein.
CONCLUSION:AICAR and/or IFN-ɑ-2b can inhibit the cell proliferation and promote the apoptosis of K562 cells. The combination of two drugs shows synergistic antitumor effect, and its mechanism may be related to the promotion of high expression of wild-type p53 protein.
