LncRNA FOXD2-AS1 regulates chondrocyte proliferation in osteoarthritis by acting as a sponge of miR-206 to modulate CCND1 expression.

Recently, accumulating evidence demonstrated that the long non-coding RNAs (lncRNAs) play important roles in osteoarthritis (OA) progression. However, the role of lncRNA FOXD2-AS1 on OA is still unclear. In the present study, qRT-PCR showed that expression of FOXD2-AS1 and Cyclin D1 (CCND1) was upregulated in OA cartilage tissues, while miR-206 expression was significantly decreased. CCK-8 and colony formation assays showed that FOXD2-AS1 could promote chondrocytes viability. Flow cytometry analysis showed that FOXD2-AS1 inhibition arrested chondrocytes in G0/G1 phase and induced cells apoptosis. Furthermore, luciferase reporter assay and RIP assay showed that FOXD2-AS1 could function as a sponge of miR-206. Rescue assays showed that miR-206 inhibitors reversed the effects of FOXD2-AS1 suppression on chondrocytes viability. In addition, we identified that CCND1 acted as a direct target of miR-206. FOXD2-AS1 suppression could inhibit CCND1 expression in chondrocytes, while miR-206 inhibitors reversed CCND1 expression. Moreover, rescue assays indicated that CCND1 overexpression reversed the effects of FOXD2-AS1 suppression on chondrocytes viability. Taken together, these data indicated that FOXD2-AS1 could promote the growth of chondrocytes by targeting miR-206/CCND1 axis.