MicroRNA let-7i induced autophagy to protect T cell from apoptosis by targeting IGF1R |
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Authors: | Chunfeng Hou Mengzhu Zhu Min Sun Yanliang Lin |
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Affiliation: | 1. Department of Rheumatology, Jining First People’s Hospital, Jining, Shandong 272111, PR China;2. Department of Rheumatology, Chinese Medicine Hospital in Linyi City, Linyi, Shandong 276000, PR China;3. Clinic Institute, Jining Medical University, Jining, Shandong 272013, PR China;4. Department of Center Laboratory, Shandong Provincial Hospital Affiliated to Shandong University, Jinan 250021, PR China |
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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. |
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Keywords: | Ankylosing Spondylitis MicroRNA let-7i IGF1R Autophagy Apoptosis |
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