Preliminary investigation of TIM-3 ligand galectin-9 inducing apoptosis of NK/T cell lymphoma cells
10.3872/j.issn.1007-385x.2018.07.006
- VernacularTitle:TIM-3配体galectin-9诱导NK/T细胞淋巴瘤细胞的凋亡及其机制
- Author:
JIANG Jifeng
1
;
LIU Chuanxu
1
;
LI Gaoyang
1
;
TAO Rong
1
Author Information
1. (Department of Hematology, Xinhua Hospital, Affiliated to School of Medicine, Shanghai Jiaotong University, Shanghai 200092, China
- Publication Type:Journal Article
- Keywords:
Natural killer/T-cell lymphoma;
T-cell immunoglobulin and mucin-domain containing-3;
Galetin-9;
Cell apoptosis
- From:
Chinese Journal of Cancer Biotherapy
2018;25(7):693-697
- CountryChina
- Language:Chinese
-
Abstract:
Objective: To identify the expression pattern of TIM-3 in natural killer/T-cell lymphoma (NK/TCL) cell lines, and to investigate the effect and mechanism of its ligand galectin-9 (GAL-9) inducing apoptosis of NK/TCL cell lines. Methods: Expression of TIM-3 in NK cell of peripheral blood from healthy donors and NK/TCL cell lines (SNK-1、SNK-6、SNT-8) was detected by Western blotting. After being treated with rhGAL-9 at various concentrations for 24h, the cell proliferation ability was analyzed with CCK-8 assay. Apoptosis ratio of the cells was determined by flow cytometry. Expressions of caspase-3, PARP and their cleavages were detected by Western blotting; moreover, phosphorylation levels of proteins in MAPK signaling pathway were also detected by Western blotting. Results: The expression of TIM-3 in SNK-1, SNK-6 and SNT-8 cell lines was significantly higher than that of NK cells from healthy donors (P<0.05). CCK-8 result showed that rhGAL-9 obviously inhibited the proliferation of NK/TCL cell lines in a concentration dependent manner. Flow cytometry showed that rhGAL-9 induced the apoptosis of NK/TCLcells; and Western blotting proved that the expression of cleaved caspase-3, cleaved-PARP, and p-JNK in MAPK signaling pathway were significantly elevated. Conclusion: TIM-3 was over-expressed in NK/TCL cell lines, and its ligand galectin-9 induced cell apoptosis probably through the activation of JNK kinase pathways.
- Full text:20180706.pdf
