Transforming growth factor-β (TGF-β) signaling plays pivotal roles in the pathogenesis of osteoarthritis, while TGF-β signaling in certain diseases models is regulated by the long noncoding RNA (lncRNA) antidifferentiation noncoding RNA (ANCR). Therefore, ANCR may also participate in osteoarthritis. In this study, the expression of ANCR and TGF-β1 in the plasma of osteoarthritis patients and healthy controls was detected by real-time quantitative polymerase chain reaction and enzyme-linked immunosorbent assay, respectively. The diagnostic value of ANCR for osteoarthritis was evaluated by receiver operating characteristic receiver operating characteristic (ROC) curve analysis. The correlation between the plasma levels of ANCR and TGF-β1 was analyzed by the Pearson correlation coefficient. The ANCR expression vector was transfected into cells of the human chondrocyte cell line CHON-001 (ATCC CRL-2846), and the effect on TGF-β1 expression and cell proliferation was detected by Western blot and cell counting kit-8 assay, respectively. We observed that the plasma levels of ANCR were significantly lower, while the plasma levels of TGF-β1 were significantly higher in osteoarthritis patients than those in healthy controls. Downregulation of ANCR effectively distinguished osteoarthritis patients from healthy controls. ANCR and TGF-β1 expression was negatively correlated in osteoarthritis patients but not in healthy controls. ANCR overexpression promoted the proliferation of chondrocytes and inhibited TGF-β1 expression. We concluded that ANCR might participate in osteoarthritis by downregulating TGF-β1 and promote the proliferation of chondrocytes.
Keywords: chondrocytes; long non-coding RNA ANCR; osteoarthritis; transforming growth factor-β1.
© 2019 Wiley Periodicals, Inc.