Effect of chidamide on human B lymphoma cell lines and its mechanisms.
- Author:
Yan-Ying LI
1
;
Yan-Fang WANG
;
Jing WANG
;
Xiao-Yan KE
Author Information
1. Department of Hematology, Peking University Third Hospital, Beijing, China.
- Publication Type:Journal Article
- MeSH:
Aminopyridines;
pharmacology;
Apoptosis;
drug effects;
Benzamides;
pharmacology;
Caspase 3;
metabolism;
Cell Line, Tumor;
Cell Proliferation;
drug effects;
Histone Deacetylase Inhibitors;
pharmacology;
Humans;
Lymphoma, B-Cell;
metabolism;
pathology
- From:
Journal of Experimental Hematology
2012;20(4):893-899
- CountryChina
- Language:Chinese
-
Abstract:
This study was aimed to explore the effects of histone deacetylase inhibitor chidamide on the proliferation, apoptosis of B lymphoma cell lines Raji (Burkitt lymphoma), Maver and Z-138 (mantle cell lymphoma) and its mechanisms. Three B lymphoma cell lines were cultured in vitro with different concentrations of chidamide for different time. The cell proliferation was determined by CCK-8 method; the cell apoptosis and mitochondrial membrane potential were analyzed by flow cytometry; the protein levels of histone H3/H4 acetylation in cells and the activity of caspase-3 were detected by Western blot. The results showed that chidamide inhibited the proliferation of 3 B lymphoma cell lines in time- and concentration-dependent manners, especially in Z-138 cell line earlier and faster; chidamide could induce cell apoptosis and decline of mitochondrial membrane potential, which was more sensitive in Maver and Z-138 cells than that in Raji cells. Chidamide could elevate the histone H3/H4 acetylation level in 3 B lymphoma cell lines and the activity of caspase-3 in Maver and Z-138 cells. It is concluded that chidamide can inhibit proliferation of B lymphoma cell lines and promote cell apoptosis, the increase of histone H3/H4 acetylation induced by chidamide, triggering of mitochondrial pathway and activation of caspase-3 may be considered as possible mechanisms.
