Circ-NFKB1 sponges miR-203a-5p to regulate ERBB4 expression and promotes IL-1β induced chondrocytes apoptosis

Osteoarthritis (OA) is a chronic disease of the bones and joints that commonly affects middle-aged and elderly individuals, characterized by the degeneration of articular cartilage and inflammation of the joints. The molecular mechanisms of OA urgently need to be further examined. Our study intended to uncover circ-NFKB1/miR-203a-5p/ERBB4 axis in regulating interleukin-1β (IL-1β) induced chondrocytes apoptosis.

GSE178724, GSE79258 and GSE169077 were downloaded from Gene Expression Omibus (GEO) database and differentially expressed circRNAs, miRNAs and mRNAs were obtained by R software. Annexin V assay was used to determine cell apoptosis rate. ELISA was further performed to identify the inflammation response. Dual-luciferase reporter gene assay was conducted to examine the combination among circ-NFKB1, miR-203a-5p and ERBB4.

Our research demonstrated that circ-NFKB1 and ERBB4 were significantly upregulated through bioinformatic analysis. MiR-203a-5p was significantly downregulated through bioinformatic analysis. Silencing of circ-NFKB1 notably inhibited the IL-1β induced chondrocytes apoptosis and upregulated ERBB4 expression. Through prediction on bioinformatics analysis, miR-203a-5p was the target binding circ-NFKB1, and ERBB4 was the potential target of miR-203a-5p. Subsequently, these changes induced by the silencing of circ-NFKB1 were reversed upon addition of pcDNA/ERBB4.

Silencing circ-NFKB1 could sponge miR-203a-5p to regulate ERBB4 expression and alleviate OA progression.