LncRNA SNHG5/miR-26a/SOX2 signal axis enhances proliferation of chondrocyte in osteoarthritis
LncRNA SNHG5/miR-26a/SOX2 signal axis enhances proliferation of chondrocyte in osteoarthritis
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DOI：
10.1093/abbs/gmx141
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发表时间：
2018-02-01
影响因子：
3.7
通讯作者：
Zhang, Ying
中科院分区：
文献类型：
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作者：
Shen, Huijun;Wang, Yue;Zhang, Ying
软骨细胞参与骨关节炎（OA）患者关节的破坏。本研究旨在探讨小核仁RNA宿主基因5 （SNHG5）在软骨细胞中的表达水平并评价其功能。本研究采用实时定量逆转录聚合酶链式反应检测了SNHG5、miR-26a和SOX2在17对关节软骨组织和非oa组中的表达水平。结果显示，在OA组织中，SNHG5和SOX2水平显著下调，miR-26a水平上调。通过MTT、集落形成和细胞transwell实验来评估SNHG5对CHON-001细胞的细胞活力、生长能力和迁移能力的作用。发现SNHG5能促进软骨细胞的增殖和迁移。SNHG5与miR-26a之间的关系通过RIP和荧光素酶报告基因检测得到证实。通过荧光素酶报告基因检测，SOX2被鉴定为miR-26a的靶基因。采用拯救实验验证SNHG5、miR-26a和SOX2之间的关系。我们目前的研究表明，SNHG5通过作为竞争性海绵miR-26a的ceRNA参与OA的机制，从而调节SOX2的表达。
Chondrocyte is involved in the destruction of joints in osteoarthritis (OA) patients. The aim of this study was to explore the expression level of small nucleolar RNA host gene 5 (SNHG5) and evaluate its function in chondrocyte. In our current study, the expression levels of SNHG5, miR-26a, and SOX2 in 17 pairs of articular cartilage tissues and in the non-OA group were assessed by real-time quantitative reverse-transcription polymerase chain reaction. Results showed that the levels of SNHG5 and SOX2 were significantly downregulated in OA tissues, while the level of miR-26a was upregulated. MTT, colony formation and cell transwell assays were performed to assess the function of SNHG5 on the cell viability, growth ability, and migration capacity in CHON-001 cells. It was found that SNHG5 could promote chondrocyte cell proliferation and migration. The relationship between SNHG5 and miR-26a was confirmed by RIP and the luciferase reporter assays. SOX2 was identified as a target gene of miR-26a by the luciferase reporter assay. Rescue assay was applied to verify the relationship among SNHG5, miR-26a, and SOX2. Our current study demonstrated that SNHG5 is involved in the mechanism of OA through functioning as a ceRNA to competitively sponge miR-26a, therefore, regulating the expression of SOX2.