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[Early apoptosis of HL-60 cells induced by anti-CD44 McAb A3D8 inhibiting ERK1/2-upregulated Bim expression].
- Source :
-
Zhongguo shi yan xue ye xue za zhi [Zhongguo Shi Yan Xue Ye Xue Za Zhi] 2011 Jun; Vol. 19 (3), pp. 656-60. - Publication Year :
- 2011
-
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.
- Subjects :
- Antibodies, Monoclonal immunology
Bcl-2-Like Protein 11
Cell Proliferation drug effects
Gene Expression Regulation, Leukemic
HL-60 Cells
Humans
Hyaluronan Receptors immunology
Mitogen-Activated Protein Kinase 1 metabolism
Mitogen-Activated Protein Kinase 3 metabolism
Up-Regulation
Antibodies, Monoclonal pharmacology
Apoptosis drug effects
Apoptosis Regulatory Proteins metabolism
Membrane Proteins metabolism
Proto-Oncogene Proteins metabolism
Subjects
Details
- Language :
- Chinese
- ISSN :
- 1009-2137
- Volume :
- 19
- Issue :
- 3
- Database :
- MEDLINE
- Journal :
- Zhongguo shi yan xue ye xue za zhi
- Publication Type :
- Academic Journal
- Accession number :
- 21729544