MicroRNA let-7i induced autophagy to protect T cell from apoptosis by targeting IGF1R

被引：43
|
作者：
Hou, Chunfeng [1 ]
Zhu, Mengzhu [2 ]
Sun, Min [3 ]
Lin, Yanliang [4 ]
机构：
[1] Jining First Peoples Hosp, Dept Rheumatol, Jining 272111, Shandong, Peoples R China
[2] Chinese Med Hosp Linyi City, Dept Rheumatol, Linyi 276000, Shandong, Peoples R China
[3] Jining Med Univ, Inst Clin, Jining 272013, Shandong, Peoples R China
[4] Shandong Univ, Shandong Prov Hosp, Dept Ctr Lab, Jinan 250021, Peoples R China
来源：
BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS | 2014年 / 453卷 / 04期
基金：
中国国家自然科学基金;
关键词：
Ankylosing Spondylitis; MicroRNA let-7i; IGF1R; Autophagy; Apoptosis; GROWTH-FACTOR-I; INSULIN-RECEPTOR SUBSTRATE; ANKYLOSING-SPONDYLITIS; RHEUMATOID-ARTHRITIS; ABERRANT EXPRESSION; CANCER PROGRESSION; DOWN-REGULATION; STEM-CELLS; DISEASE; INFLAMMATION;
D O I：
10.1016/j.bbrc.2014.10.002
中图分类号：
Q5 [生物化学]; Q7 [分子生物学];
学科分类号：
071010 ; 081704 ;
摘要：
MicroRNA let-7i is up-regulated in T cells from patients with Ankylosing Spondylitis (AS). In this study, we investigated the role of let-7i in T cells survival. Our results demonstrated down-regulation of insulin-like growth factor-1 receptor (IGF1R) in T cells from patients with AS. Luciferase reporter assay suggested IGF1R as direct target of let-7i. Overexpression of let-7i in Jurkat cells significantly suppressed IGF1R expression, which mimicked the action of IGF1R siRNA. IGF1R inhibition led to a strinking decrease in phosphorylation of mTOR and Akt, down-regulation of Bcl-2, up-regulation of Bax and cleavage of caspase 3 and PARP. Meanwhile, IGF1R inhibition induced autophagy. Autophagy induced by let-7i overexpression contributed to protect cells from apoptosis. Our data indicated that let-7i might control T cells fates in AS by targeting IGF1R. (C) 2014 Elsevier Inc. All rights reserved.
引用
收藏
页码：728 / 734
页数：7
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