Effect of LncRNA Cancer Upregulated Drug Resistant (CUDR) on Osteoarthritis Chondrocyte Proliferation and Apoptosis by Regulating NF-κB Signaling Pathway

Abstract

Osteoarthritis (OA) is a common and frequently-occurring disorder in orthopedics. LncRNA CUDR involves in several physiological and pathological activities of the body. However, the role and mechanism of LncRNA CUDR in OA has not been elucidated. Cartilage tissue from OA patients and normal bone and joints were collected to detect LncRNA CUDR level by Real-time PCR. Chondrocytes from OA patients were isolated and divided into control group, LncRNA CUDR siRNA group, and LncRNA CUDR group followed by analysis of cell proliferation by MTT assay, Caspase 3 activity, NF-κB expression by Western blot, secretion of TNF-α and IL-6 by ELISA. LncRNA CUDR was significantly higher in OA patients than controls (P <0.05). LncRNA CUDR siRNA transfection into OA chondrocytes can significantly down-regulate LncRNA CUDR expression, promote cell proliferation, and reduce Caspase 3 activity, NF-κB level, as well as TNF-α and IL-6 secretion (P <0.05). Transfection of pcDNALncRNA CUDR plasmid into OA chondrocytes could up-regulate the expression of LncRNA CUDR and significantly reverse the above changes (P <0.05). LncRNA CUDR expression is increased in OA patients. Down-regulating LncRNA CUDR can inhibit the apoptosis and promote proliferation of articular chondrocytes and inhibit arthritis by down-regulating the NF-κB signaling pathway