LncRNA MIR4435‑2HG inhibits the progression of osteoarthritis through miR‑510‑3p sponging

Abstract

Osteoarthritis (OA) is a disorder of diarthrodial joints that can have multiple causes. Long non‑coding RNAs (lncRNAs) participate in multiple diseases, including OA. It has recently been reported that the lncRNA microRNA 4435‑2HG (MIR4435‑2HG) is downregulated in OA tissues; however, the biological role of MIR4435‑2HG during OA progression remains unclear. In the present study, interleukin (IL)‑1β was used to establish an in vitro model of OA. Protein expressions of matrix metallopeptidase (MMP) 1, MMP13, collagen II, interleukin (IL)‑17A, p65, phosphorylated (p)‑p65, IκB and p‑IκB in CHON‑001 cells were detected by western blotting. Gene expressions of IL‑17A, MIR4435‑2HG and miR‑510‑3p in tissues or CHON‑001 cells were measured by reverse transcription‑quantitative PCR and western blotting, respectively. Cell Counting Kit‑8 assay and immunofluorescence staining were used to investigate cell proliferation, and cell apoptosis was detected by flow cytometry. The association between MIR4435‑2HG, miR‑510‑3p and IL‑17A was investigated using the dual luciferase report assay. MIR4435‑2HG and miR‑510‑3p overexpression were transfected into CHON‑001 cells. The results demonstrated that miR4435‑2HG overexpression significantly increased proliferation and inhibited apoptosis of CHON‑001 cells. In addition, miR‑510‑3p was identified as the downstream target of MIR4435‑2HG, and miR‑510‑3p directly targeted IL‑17A. The results from the present study suggested that MIR4435‑2HG could mediate the progression of OA by inactivating the NF‑κB signaling pathway. In addition, miR4435‑2HG overexpression inhibited OA progression, suggesting that miR4435‑2HG may be considered as a potential therapeutic target in OA.

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