Role of Extracelluar Regulated Protein Kinases in FTY720-induced Apoptosis of Leukemia Cell Lines HL-60 and U937

• Published in: Journal of Huazhong University of Science and Technology. Medical sciences Vol. 24; no. 1; pp. 45 - 47
• Main Author: 李登举 张瑶珍 胡向荣 曹文静 黄伟
• Format: Journal Article
• Language: English
• Published: China Department of Hematology, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology,Wuhan 430030 2004
• Subjects: Apoptosis - drug effects; Cell Division - drug effects; Extracellular Signal-Regulated MAP Kinases - metabolism; Fingolimod Hydrochloride; FTY720; HL-60 Cells; HL-60细胞; Humans; Immunosuppressive Agents - pharmacology; Mitogen-Activated Protein Kinase 1 - metabolism; Mitogen-Activated Protein Kinase 3 - metabolism; Phosphorylation; Propylene Glycols - pharmacology; Signal Transduction; Sphingosine - analogs & derivatives; U937 Cells; U937细胞; 免疫抑制; 免疫疗法; 白血病; 细胞凋亡; 细胞外调节激酶; leukemia; apoptosis; extracelluar regulated protein kinase; FTY720; proliferation inhibition
• ISSN: 1672-0733; 1993-1352

The effects of a novel immunosuppressive agent FTY720 on proliferation inhibition and apoptosis of acute leukemia cell lines HL-60 and U937, and the role of extracelluar regulated protein kinase (ERK) in the course of proliferation inhibition and apoptosis induced by FTY720 were studied. The proliferation inhibition rate of HL-60 and U937 cells by various concentrations of FTY720 was detected by MTT assay. Cell apoptosis was detected by DNA fragmem analysis and flow cytometry. The phosphorylated ERK1/2 protein expression was observed by Western blotting. The change of intracellular distribution of ERK1/2 protein was identified by SP immunohistochemical staining. The results showed that FTY720 could inhibit the growth of HL-60 and U937cells effectively in a dose-dependent manner. After incubation with FTY720 for 24 h, apoptosis wasobserved in HL-60 and U937 cells. The intracellular expression of phosphorylated ERK1/2 protein was also down-regulated and the distribution of ERK1/2 protein in cell' nuclear was reduced during FTY720-induced apoptosis. So, that FTY720 inhibited ERK1/2 phosphorylation might mediate the role of FTY720-induced apoptosis and proliferation inhibition of leukemia cells.