Early apoptosis of HL-60 cells induced by anti-CD44 McAb A3D8 inhibiting ERK1/2-upregulated Bim expression.
- Author:
Guo-Qiang CHANG
1
;
Jian WANG
;
Wei GAO
;
Ruo-Jun WANG
;
Li-Hong WANG
;
Wei-Na JIN
;
Ya-Ni LIN
;
Hua-Wen LI
;
Tian-Xiang PANG
Author Information
1. State Key Laboratory of Experimental Hematology, Institute of Hematology & Blood Disease Hospital, Chinese Academy of Medical Sciences & Peking Union Medical College, Tianjin 300020, China.
- Publication Type:Journal Article
- MeSH:
Antibodies, Monoclonal;
immunology;
pharmacology;
Apoptosis;
drug effects;
Apoptosis Regulatory Proteins;
metabolism;
Bcl-2-Like Protein 11;
Cell Proliferation;
drug effects;
Gene Expression Regulation, Leukemic;
HL-60 Cells;
Humans;
Hyaluronan Receptors;
immunology;
Membrane Proteins;
metabolism;
Mitogen-Activated Protein Kinase 1;
metabolism;
Mitogen-Activated Protein Kinase 3;
metabolism;
Proto-Oncogene Proteins;
metabolism;
Up-Regulation
- From:
Journal of Experimental Hematology
2011;19(3):656-660
- CountryChina
- Language:Chinese
-
Abstract:
This study was aimed to investigate the effects of anti-CD44 mAb A3D8 on proliferation and apoptosis of AML cells, to explore the mechanism of ERK1/2 and Bim in this process. Effect of the anti-CD44 mAb A3D8 on the HL-60 cell proliferation was assayed with MTT method, the change of mitochondrial transmembrane potential of HL-60 cells was analyzed by flow cytometry. The mRNA expression of Bim was determined by real-time quantitative RT-PCR. Western blot was used to detect the protein expression of p-ERK1/2. The results showed that mAb A3D8 could remarkably inhibit the proliferation capacity of the HL-60 cells in a dosage- and time-dependent ways. The mitochondrial transmembrane potential in HL-60 cells treated with A3D8 (3.0 µg/ml) was significantly decreased as compared with the control cells. Furthermore, the mRNA expression of Bim was much higher than that in controls. Expression of the p-ERK was much lower than that of the controls. It is concluded that anti-CD44 mAb A3D8 can inhibit the proliferation and induce the apoptosis of HL-60 cells, mechanism of which is enhancing the expression of Bim via inhibiting p-ERK1/2.
