Effect of SHIP1 on viability and apoptosis of leukemia Jurkat cells by reg-ulating STAT3 signaling pathway
10.3969/j.issn.1000-4718.2018.01.015
- VernacularTitle:SHIP1调控STAT3信号通路对白血病Jurkat细胞活力和凋亡的影响
- Author:
Peng FANG
1
;
Nuo-Fang ZHANG
Author Information
1. 河南省开封市儿童医院PICU
- Keywords:
Leukemia;
SH2 domain-containing inositol 5-phosphatase 1;
Cell viability;
Apoptosis;
STAT3 signaling pathway
- From:
Chinese Journal of Pathophysiology
2018;34(1):87-93
- CountryChina
- Language:Chinese
-
Abstract:
AIM:To investigate the effect of SH2 domain-containing inositol 5-phosphatase 1(SHIP1)on the viability and apoptosis of leukemia cells by regulating signal transducer and activator of transcription 3(STAT3)signaling pathway.METHODS:Human leukemia Jurkat cells were transfected with null vector and SHIP1 overexpression vector in negative control(NC)group and SHIP1 group,respectively.The cells without treatment served as control group.The transfection efficiency was detected by real-time PCR and Western blot.The changes of the cell activity were measured by MTT assay.The apoptosis was detected by flow cytometry.The protein levels of cleaved caspase-3,STAT3 and p-STAT3 were determined by Western blot.The STAT3 signaling pathway inhibitor AG 490 was applied to the cells in control group and SHIP1 group as control +AG490 group and SHIP1+AG490 group,respectively,and the above indexes were also ana-lyzed.RESULTS:Compared with the control group and NC group ,the mRNA and protein expression levels of SHIP 1 in SHIP1 group were both upregulated ,the cell viability was increased ,the apoptotic rate was decreased ,the protein level of cleaved caspase-3 was upregulated ,and the protein level of p-STAT3 was decreased(P<0.05 ).Compared with control group and control +AG490 group,the cell viability in SHIP1+AG490 group was decreased ,the protein level of cleaved caspase-3 was increased the protein level of p-STAT3 was decreased ,and the apoptotic rate was increased(P<0.05 ). CONCLUSION:SHIP1 inhibits the viability and promotes the apoptosis of human leukemia Jurkat cells by inhibiting the STAT3 signaling pathway.
