LncRNA-p21 promotes chondrocyte apoptosis in osteoarthritis by acting as a sponge for miR-451

Osteoarthritis (OA) is the most common type of arthritis, and remains to be social and medical challenge. Thus, identifying novel molecular targets is important for the prevention and treatment of OA. Long noncoding RNAs (lncRNAs) have been reported to modulate various biological and pathological processes. The aim of the present study was to investigate the role of lncRNA-p21 in OA and its underlying mechanism, in order to better understand the development of OA and its treatment. Chondrocytes were isolated from cartilage samples obtained from OA and normal patients. Chondrocytes were transfected with microRNA (miRNA/miR)-451 mimics, miR-451 inhibitor, pcDNA3.1(+)-p21 or small interfering RNA-p21. Flow cytometry was performed to analyze cell apoptosis and reverse transcription-quantitative polymerase chain reaction was conducted to detect the expression of mRNAs and miRNAs. Cell Counting Kit-8 assay was performed to detect cell viability. The results revealed that the level of lncRNA-p21 was significantly upregulated in OA cartilage when compared with the normal cartilage. Silencing of lncRNA-p21 increased cell viability and inhibited the apoptosis rate of chondrocytes in OA, while lncRNA-p21 overexpression decreased cell viability and increased the apoptosis rate of chondrocytes in OA. Overexpression of lncRNA-p21 suppressed the expression of miR-451 while the silencing of lncRNA-p21 reversed this effect. MiR-451 inhibitor effectively inhibited the upregulatory effect of si-p21 on miR-451. The increased cell viability and decreased apoptosis rate induced by lncRNA-p21 silencing was abolished by the miR-451 inhibitor. MiR-451 mimic effectively increased the downregulatory effect of pcDNA3.1-lncRNA-p21 on miR-451. The decreased cell viability and increased apoptosis rate induced by the overexpression of lncRNA-p21 was abolished by the miR-451 mimic. Investigation into the underlying mechanism revealed that lncRNA-p21 interacted with miRNA-451. In addition, lncRNA-p21 negatively regulated the expression of miR-451. Furthermore, lncRNA-p21 promoted the apoptosis of chondrocytes in OA by acting as a sponge for miR-451. Thus, lncRNA-p21 was proposed as a promising target for the treatment of OA.