Mechanisms of ROS in U266 cell death induced by FTY720.
10.7534/j.issn.1009-2137.2013.03.021
- Author:
Ying-Chun LI
1
;
Zhuo-Gang LIU
;
Kun YAO
;
Hui-Han WANG
;
Rong HU
;
Wei YANG
;
Ai-Jun LIAO
Author Information
1. Department of Hematology, China Medical University, Shenyang, Liaoning Province, China.
- Publication Type:Journal Article
- MeSH:
1,2-Dihydroxybenzene-3,5-Disulfonic Acid Disodium Salt;
Apoptosis;
drug effects;
Autophagy;
drug effects;
Cell Line, Tumor;
Fingolimod Hydrochloride;
Humans;
Macrolides;
Microtubule-Associated Proteins;
metabolism;
Multiple Myeloma;
metabolism;
pathology;
Propylene Glycols;
pharmacology;
Reactive Oxygen Species;
metabolism;
Sphingosine;
analogs & derivatives;
pharmacology
- From:
Journal of Experimental Hematology
2013;21(3):643-646
- CountryChina
- Language:Chinese
-
Abstract:
This study was purpose to investigate the role of reactive oxygen species (ROS) in apoptosis and autophagy induced by FTY720 in multiple myeloma cell line U266. U266 cells were treated by different concentrations of FTY720 for 24 h, the apoptotic rates were detected by flow cytometry, and the expression of LC3B was detected by Western blot. The results indicated that apoptosis and autophagy were induced by FTY720 in U266 cells. Autophagy induced by FTY720 could lead to cell death. Bafilomycin A1, the inhibitor of autophagy, could enhance the cell viability in U266 cells treated with FTY720. NAC or Tiron, ROS scavenger, could decrease the FTY720 induced apoptosis and the expression of LC3B-II was reduced in combination of FTY720 with NAC or Tiron as compared with treatment with FTY720 only. It is concluded that FTY720 can induce U266 cell apoptosis and autophagy. ROS is the mediator that regulates both the apoptosis and autophagy in multiple myeloma cells.
