LncRNA THUMPD3-AS1 enhances the proliferation and inflammatory response of chondrocytes in osteoarthritis

Objective: Long noncoding RNAs (lncRNAs) regulate the occurrence and development of osteoarthritis (OA), whereas the biological roles and mechanisms of the lncRNA THUMPD3-AS1 (THUMPD3 antisense RNA 1) in OA remain still unclear. This study described the role and molecular mechanism of lncRNA THUMPD3-AS1 in regulating OA biology. Method: The knee normal and OA cartilage tissues from ten participants were sequenced to reveal the differentially expressed lncRNAs. The interleukin (IL)-1 beta-stimulated C28/I2 cell served as OA cells. Flow cytometry assays, Western blot, enzyme-linked immunosorbent assays were used for our experiments. Results: The results revealed that lncRNA THUMPD3-AS1 was downregulated in OA cartilage tissues and IL-1 beta stimulated chondrocyte cell line. Overexpression of lncRNA THUMPD3-AS1 alleviated cell apoptosis and facilitated inflammatory responses, whereas knockdown had opposite effects. LncRNA THUMPD3-AS1 markedly increased the cyclin E2, cyclin-dependent kinase 4, B-cell lymphoma 2, tumor necrosis factor-alpha, nitric oxide, and IL-6 levels, and decreased the caspase-3 level. Furthermore, the target proteins of phosphorylation were identified as nuclear factor-Kappa B p65 and mitogen-activated protein kinase p38, which could be indirectly suppressed by lncRNA THUMPD3-AS1 knockdown. Conclusion: Our findings highlight the different effects of lncRNA THUMPD3-AS1 on cell apoptosis and inflammatory response, which extend the multiple functions of lncRNA epigenetics in OA biology.