Hyperactivation of c-Jun NH(2)-terminal protein kinase contributes to the proliferation of B lymphoma cells.
- Author:
Yuan-Yuan GUO
1
;
Jian CUI
;
Chun-Mei HOU
;
Qing-Yang WANG
;
Jing WANG
;
Yuan-Fang MA
;
Ji-Yan ZHANG
Author Information
1. Department of Molecular Immunology, Academy of Military Medical Sciences, Beijing 100850, China.
- Publication Type:Journal Article
- MeSH:
Cell Line, Tumor;
Cell Proliferation;
Humans;
JNK Mitogen-Activated Protein Kinases;
metabolism;
Lymphoma, B-Cell;
metabolism;
pathology
- From:
Journal of Experimental Hematology
2011;19(1):100-104
- CountryChina
- Language:Chinese
-
Abstract:
This study was purposed to explore the effect of hyperactivation of c-Jun NH(2)-terminal protein kinase (JNK) on the proliferation of B lymphoma cells. The human B lymphoma cell lines Daudi and Raji were chosen as research objects. The expression of JNK protein was determined by Western blot. The subcellular localization of JNK protein was detected by immunofluorescence. The cell cycle was analyzed by flow cytometry. The suppressive effect of JNK inhibitor SP600125 on the proliferation of Daudi and Raji cells was assayed by ATPLite method. The results demonstrated that hyperactivation of JNK has been found in Daudi and Raji cells. Immunofluorescence confirmed the aberrant subcellular localization of JNK protein in Daudi and Raji cells. Cell cycle assay revealed that Daudi and Raji cells underwent G(2)-M arrest in the presence of SP600125. Furthermore, Daudi and Raji cells showed significant increase in sub-G(1) population, an indicator of apoptotic cells, with the treatment of JNK inhibitors. These data suggested that JNK inhibitors suppressed the growth of B lymphoma cells via cell cycle arrest and apoptosis. Daudi and Raji cells treated with different concentrations of JNK selective inhibitor SP600125 showed dose-dependent reduction in the growth of Daudi and Raji cells. It is concluded that hyperactivation of JNK enhance the proliferation of Daudi and Raji cells. The aberrant subcellular localization of JNK protein may facilitate the nuclear accumulation of basal JNK activity, which made JNK to be a potential target to treat human B lymphoma.
