LncRNA SNHG5/miR-26a/SOX2 signal axis enhances proliferation of chondrocyte in osteoarthritis
Huijun Shen1, Yue Wang2, Wudan Shi1
1Department of Hematology and Rheumatology, The Fourth Affiliated Hospital of Harbin Medical University, Harbin 150081, China.
Abstract:
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.
Insights
Small nucleolar RNA host gene 5 (SNHG5) promotes chondrocyte proliferation and migration in osteoarthritis. SNHG5 acts as a ceRNA, regulating SOX2 via sponging miR-26a.
Area of Science:
- Biomedical research
- Molecular biology
- Osteoarthritis research
Background:
- Chondrocytes play a critical role in joint destruction in osteoarthritis (OA).
- Understanding the molecular mechanisms underlying OA pathogenesis is crucial for developing effective treatments.
Purpose of the Study:
- To investigate the expression levels of small nucleolar RNA host gene 5 (SNHG5) in OA.
- To elucidate the functional role of SNHG5 in chondrocytes and its regulatory network.
Main Methods:
- Real-time quantitative reverse-transcription polymerase chain reaction (RT-qPCR) for gene expression analysis.
- Cellular assays including MTT, colony formation, and transwell assays to assess chondrocyte function.
- RNA immunoprecipitation (RIP) and luciferase reporter assays to confirm molecular interactions.
Main Results:
- SNHG5 and SOX2 expression were significantly downregulated in OA cartilage tissues, while miR-26a was upregulated.
- SNHG5 overexpression promoted chondrocyte proliferation and migration.
- SNHG5 functions as a competing endogenous RNA (ceRNA) for miR-26a, which targets SOX2.
Conclusions:
- SNHG5 plays a protective role in osteoarthritis by promoting chondrocyte function.
- The SNHG5/miR-26a/SOX2 axis represents a potential therapeutic target for osteoarthritis.
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