CircSEC24A promotes IL‐1β‐induced apoptosis and inflammation in chondrocytes by regulating miR‐142‐5p/SOX5 axis

Background Osteoarthritis (OA) is a common joint disease. Currently, many studies have revealed that circular RNAs (circRNAs) are strongly related to the occurrence and development of diseases. Hence, we aimed to further elucidate the role and molecular mechanism of circRNA SEC24 homolog A, COPII coat complex component (circSEC24A) in OA. Methods Chondrocytes were treated with interleukin-1β (IL-1β) to establish OA cell model in vitro. The expression levels of circSEC24A, microRNA-142-5p (miR-142-5p), and sex-determining region Y-box protein 5 (SOX5) were determined by quantitative real-time polymerase chain reaction. MTT and colony formation assays were used to determine cell proliferation. Cell apoptosis was detected by flow cytometry analysis. The protein levels of inflammatory factors and SOX5 were determined by western blot assay. The relationship between miR-142-5p and circSEC24A or SOX5 was confirmed using dual-luciferase reporter assay and RNA immunoprecipitation assay. Results CircSEC24A and SOX5 expression were enhanced, while miR-142-5p level was reduced in OA cartilage tissues and chondrocytes. Overexpression of circSEC24A promoted IL-1β-induced injury through decreasing cell proliferation and increasing apoptosis and inflammation in chondrocytes. MiR-142-5p was a direct target of circSEC24A, and its upregulation ameliorated IL-1β-induced injury and abated the effect of oe-circSEC24A in IL-1β-induced chondrocytes. Additionally, SOX5 was a downstream target of miR-142-5p, and its overexpression had a similar role with oe-circSEC24A and reversed the impact of miR-142-5p in IL-1β-induced chondrocytes. CircSEC24A acted as a molecular sponge of miR-142-5p to regulate SOX5 expression in chondrocytes. Conclusion CircSEC24A aggravated IL-1β-induced injury via modulating miR-142-5p/SOX5 axis, providing possible targets for the clinical diagnosis and treatment of OA.