lncRNA SNHG16 promotes the occurrence of osteoarthritis by sponging miR‑373‑3p

Abstract

Osteoarthritis (OA) is a common age-related joint disorder, for which no effective disease-modifying drugs are currently available. Long non-coding RNAs (lncRNAs) are involved in the occurrence of OA. lncRNA small nucleolar RNA host gene 16 (SNHG16) has been reported to regulate inflammation; however, the exact biological function of SNHG16 in OA and its underlying mechanism of action remain unclear. In this study, gene and protein expression levels were detected using reverse transcription-quantitative PCR and western blotting, respectively. Cell apoptosis was analyzed using flow cytometry and ELISA was performed to detect TNF-α levels. The interactions between lncRNA SNHG16 and microRNA (miR)-373-3p were examined using the dual-luciferase reporter assay. lncRNA SNHG16 was upregulated in OA tissue compared with normal joint tissue. The expression levels of collagen II were significantly reduced in OA tissue compared with normal tissue. Similarly, aggrecan expression levels were significantly reduced in IL-1β-treated CHON-001 cells compared with the controls. In addition, the protein expression levels of MMP13 were significantly increased in OA tissues and IL-1β-treated CHON-001 cells compared with the controls. SNHG16 knockdown significantly increased the expression levels of aggrecan, and decreased the expression levels of MMP13, cleaved caspase-3 and p21 in IL-1β-treated CHON-001 cells. In addition, IL-1β induced CHON-001 cell apoptosis, while SNHG16 knockdown decreased IL-1β-induced apoptosis. Furthermore, the luciferase activity assay suggested that SNHG16 negatively regulated miR-373-3p in OA. Finally, the results suggested that the proinflammatory effect of IL-1β on CHON-001 cells was significantly reduced by SNHG16 knockdown. In conclusion, lncRNA SNHG16 knockdown significantly limited the progression of OA by sponging miR-373-3p in vitro, which suggested that SNHG16 may serve as a potential therapeutic target for OA.

Knockdown of LINC01138 protects human chondrocytes against IL‐1β‐induced damage by regulating the hsa‐miR‐1207‐5p/KIAA0101 axis

“…For example, lncRNA SNHG7 bind to miR‐34a‐5p to regulate cell proliferation, apoptosis, and autophagy by targeting SYVN1 30 . Downregulation of lncRNA SNHG16 remarkably inhibits the progression of OA by sponging miR‑373‑3p 31 . In the present study, LINC01138 was found to be an upstream regulator of hsa‐miR‐1207‐5p.…”

“…30 Downregulation of lncRNA SNHG16 remarkably inhibits the progression of OA by sponging miR-373-3p. 31 In the present study, LINC01138 was found to be an upstream regulator of hsa-miR-1207-5p. Silencing LINC01138 protected chondrocytes from IL-1β-induced ECM degradation and inflammation by regulating hsa-miR-1207-5p.…”

Epigenetics in Knee Osteoarthritis: A 2020–2023 Update Systematic Review

“…Fan H et al [27] found that lncRNA SNHG16 is up-regulated in KOA tissues compared to normal joint tissue, while SNHG16 knockdown significantly decreases apoptosis by down-regulating the expression level of cleaved caspase-3. Additionally, one study [28] highlighted the pro-apoptotic role of lncRNA PCAT-1 through expression of miR-27-3p.…”

Epigenetic Regulation in Knee Osteoarthritis

“…Other lncRNA and miRNA interaction modes are more unique. Through spatial conformation, the secondary structure created by lncRNA can exert a sponge-like adsorption effect on miRNA, alter the actual contact concentration of miRNA, and the production of inflammatory genes or transcription factors in OA tissue (Chen et al, 2020a;Liu et al, 2020a;Zhou et al, 2021;Fan et al, 2021;Jiang et al, 2021).…”