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

Abstract

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.

• Authors: Chunfeng Hou, Mengzhu Zhu, Min Sun, Yanliang Lin
• Journal: Biochemical and biophysical research communications (Biochem Biophys Res Commun) Vol. 453 Issue 4 Pg. 728-34 (Oct 31 2014) ISSN: 1090-2104 [Electronic] United States
• PMID: 25305490 (Publication Type: Journal Article, Research Support, Non-U.S. Gov't)
• Copyright: Copyright © 2014 Elsevier Inc. All rights reserved.

Chemical References

• MIRNLET7 microRNA, rat
• MicroRNAs
• Receptor, IGF Type 1

Topics

• Apoptosis (drug effects, genetics)
• Autophagy
• Cells, Cultured
• Gene Silencing
• Gene Targeting (methods)
• Humans
• MicroRNAs (genetics, pharmacology)
• Receptor, IGF Type 1 (genetics)
• Spondylitis, Ankylosing (genetics, pathology)
• T-Lymphocytes (drug effects, pathology)