LncRNA EPIC1 protects human osteoblasts from dexamethasone-induced cell death

被引：33
|
作者：
Zhang, Xiang-yang [1 ,2 ]
Shan, Hua-jian [1 ]
Zhang, Peng [1 ]
She, Chang [1 ]
Zhou, Xiao-zhong [1 ]
机构：
[1] Soochow Univ, Affiliated Hosp 2, Dept Orthoped, Suzhou, Peoples R China
[2] Shanghai Jiao Tong Univ, Tongren Hosp, Dept Orthoped, Sch Med, Shanghai, Peoples R China
来源：
BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS | 2018年 / 503卷 / 04期
基金：
中国国家自然科学基金;
关键词：
LncRNA; EPIC1; Osteoblasts; Dexamethasone; Myc; INDUCED APOPTOSIS; OXIDATIVE STRESS; MYC; GLUCOCORTICOIDS; ACTIVATION; MECHANISMS; INHIBITOR; DAMAGES; KINASE;
D O I：
10.1016/j.bbrc.2018.06.146
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：
Dexamethasone (Dex) can induce injury to human osteoblasts. Long non-coding RNA (LncRNA) EPIC1 (Lnc-EPIC1) is a novel Myc-interacting LncRNA. Its effect on Dex-treated human osteoblasts is studied here. In OB-6 osteoblastic cells and primary human osteoblasts, treatment with Dex increased expression of Lnc-EPIC1. Its expression is also elevated in the necrotic femoral head tissues of Dex-taking patients. Ectopic overexpression of Lnc-EPIC1 inhibited Dex-induced apoptosis and programmed necrosis in OB-6 cells and primary human osteoblasts. Reversely, Lnc-EPIC1 silencing by targeted siRNA potentiated Dex-induced cytotoxicity. Myc is the target of Lnc-EPIC1 in osteoblasts. Exogenous overexpression of Myc protected OB-6 cells from Dex. Conversely, Myc knockout by CRISPR-Cas-9 method abolished Lnc-EPIC1-induced OB-6 cytoprotection against Dex. Together, Lnc-EPIC1 expression protects human osteoblasts from Dex possible via regulation of Myc. (C) 2018 Elsevier Inc. All rights reserved.
引用
收藏
页码：2255 / 2262
页数：8
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