Effect of arsenic trioxide on induction of apoptosis in MCL cell line and its possible mechanisms.
- Author:
Ai-Mei FEI
1
;
Chao-Ming MAO
;
Jing-Jing LIU
;
Jiang ZHU
;
Jian-Qing MI
Author Information
1. State Key Laboratory of Medical Genomics, Shanghai Institute of Hematology, Department of Hematology, Shanghai Ruijin Hospital, Shanghai Jiaotong University School of Medcine, Shanghai 200025, China.
- Publication Type:Journal Article
- MeSH:
Apoptosis;
drug effects;
Apoptosis Regulatory Proteins;
metabolism;
Arsenicals;
pharmacology;
Cell Line, Tumor;
Cell Proliferation;
drug effects;
Gene Expression Regulation, Neoplastic;
Humans;
Lymphoma, Mantle-Cell;
metabolism;
Membrane Potential, Mitochondrial;
Mitochondria;
drug effects;
Oxides;
pharmacology
- From:
Journal of Experimental Hematology
2010;18(4):909-913
- CountryChina
- Language:Chinese
-
Abstract:
This study was aimed to explore the effect of arsenic trioxide (ATO) on proliferation and apoptosis of mantle cell lymphoma (MCL) cell lines and the underlying mechanisms of the apoptosis. MCL cell lines (jeko-1, mino, JVM-2) were treated with different concentrations of ATO, then growth profile of these cells were detected by MTT. Apoptosis of ATO-treated jeko-1 cells were detected by flow cytometry with Annexin V-FITC/PI double staining. The loss of mitochondrial membrane potential of ATO-treated jeko-1 cells were detected by FCM with DiOC₆(3) staining. The expressions of cyclin D1 and apoptosis related proteins MCL-1, BCL-2, PUMA, NOXA, cCaspase-3 (cleaved caspase-3), cCaspase-9 (cleaved caspase-9), cPARP (cleaved PARP) were detected by Western blot. The results indicated that ATO inhibited cell growth, induced apoptosis of MCL cells and disrupted mitochondrial membrane potential. ATO could decrease expressions of MCL-1, PUMA and cyclin D1, increase expressions of cPARP, cCaspase-3, cCaspase-9 and the expressions of BLC-2 and NOXA were not changed. It is concluded that ATO can induce cell growth arrest and apoptosis of MCL cells. The mitochondrial pathway plays a very important role in cell apoptosis.
