Upregulation of long noncoding TNFSF10 contributes to osteoarthritis progression through the miR‐376‐3p/FGFR1 axis

摘要: Osteoarthritis (OA) is a common joint disease with high morbidity, but there still no definitive treatment for it. Long noncoding RNAs (lncRNAs) have been confirmed to play key roles in OA progression. This work was done investigate the and action mechanism of lncRNA TNFSF10 OA. The messenger RNA levels articular cartilage samples from patients or chondrocytes were detected by Quantitative real-time PCR assay (qRT-PCR). effects on evaluated basis cell growth, apoptosis, inflammation. Then, interaction between miR-376-3p explored dual-luciferase reporter test, RNA-binding protein immunoprecipitation, pull-down assay. Finally, various experiments, Western blot analysis, qRT-PCR performed study among TNFSF10, miR-376-3p, fibroblast growth factor receptor 1 (FGFR1). It found that upregulated cartilages stimulated proliferation, antiapoptosis, inflammation chondrocytes. In addition, acted as competing endogenous downregulate influence partly reversed miR-376-3p. Moreover, FGFR1, target had reversal functions outcomes mediated further analysis displayed negative relationship well while FGFR1 positively related TNFSF10. Altogether, overexpression probably proliferation inflammation, inhibited apoptosis regulating miR-376-3p/FGFR1 axis, implying its increase contributed Our provided new potential biomarker therapeutic target-TNFSF10, which helpful develop an efficient approach cure