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pmid:37491357
Circ-NFKB1 sponges miR-203a-5p to regulate ERBB4 expression and promotes IL-1β induced chondrocytes apoptosis.
Zhao Wang · Hongwei Bao · Jingzhao Hou · Bin Ju · Yong Ji
Journal of orthopaedic surgery and research · 2023 doi:10.1186/s13018-023-03990-4
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Experiment
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Complete file
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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.\nMETHODS: 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.\nRESULTS: 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.\nCONCLUSIONS: Silencing circ-NFKB1 could sponge miR-203a-5p to regulate ERBB4 expression and alleviate OA progression.", "claims": [{"id": "claim-method", "statement": "The microarray data was normalized using Bioconductor's fRMA package in R and subsequently differentially expressed circRNAs, miRNAs and mRNAs were analyzed with the R limma package. 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