Department of Hematology and Rheumatology, The Fourth Affiliated Hospital of Harbin Medical University, Harbin 150081, China.
Department of Pharmacology and Toxicology Boonshoft School of Medicine, Wright State University, Fairborn OH 45435, USA.
Acta Biochim Biophys Sin (Shanghai). 2018 Feb 1;50(2):191-198. doi: 10.1093/abbs/gmx141.
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.
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)的表达水平及其在软骨细胞中的功能。在本研究中,通过实时定量逆转录聚合酶链反应评估了 17 对关节软骨组织和非 OA 组中 SNHG5、miR-26a 和 SOX2 的表达水平。结果表明,OA 组织中 SNHG5 和 SOX2 的水平显著下调,而 miR-26a 的水平上调。MTT、集落形成和细胞迁移实验评估了 SNHG5 对 CHON-001 细胞活力、生长能力和迁移能力的功能。结果发现,SNHG5 可促进软骨细胞增殖和迁移。通过 RIP 和荧光素酶报告实验证实了 SNHG5 与 miR-26a 之间的关系。荧光素酶报告实验鉴定 SOX2 是 miR-26a 的靶基因。通过 rescue 实验验证了 SNHG5、miR-26a 和 SOX2 之间的关系。本研究表明,SNHG5 通过作为 ceRNA 竞争性地吸附 miR-26a,从而调节 SOX2 的表达,参与 OA 的发生机制。