Effects of SNORD3 knockdown and over expression on Fibroblast-Like Synoviocytes

Rheumatoid arthritis (RA) is a chronic autoimmune disease characterized by systemic inflammation, synovial hyperplasia, and the destruction of bone and cartilage. Despite the use of various immunosuppressive disease-modifying antirheumatic drugs (DMARDs), a considerable proportion of RA patients remain symptomatic. As RA progresses, fibroblast-like synoviocytes (FLSs) undergo a phenotypic transition to an aggressive state, making them attractive non-immune cellular targets for RA treatment. However, there are currently no clinically available therapies that selectively ablate RA-FLSs due to the lack of specific molecular targets. Our research focuses on the knockdown and overexpression of the SNORD3 gene in RA-FLSs. SNORD3 is expressed in the cell of RA-FLSs and plays a crucial role in their aggressive transition. By specific knockout or overexpression of NCL, we observed significant aggressive transformations of RA-FLS. To investigate whether SNORD3 plays a critical role in the tumor-like transformation and overactivation of RA-FLSs, we established two RA-FLSs stable line in which the target gene was silenced down or expressed.