Role of RP11-83J16.1, a novel long non-coding RNA, in rheumatoid arthritis.

This study aimed to explore the effects of long non-coding RNA (lncRNA) expression on rheumatoid arthritis (RA). LncRNA expression profiles were obtained from the synovial tissues of five RA patients and five age-/gender-matched controls by RNA-Seq. Six candidate lncRNAs were then chosen and their levels in synovial fluid further examined in 25 RA patients and 25 health controls using RT-qPCR. The effects of lncRNA RP11-83J16.1 overexpression and knockdown on RA fibroblast-like synoviocytes (RA-FLS) function, inflammation state, and URI1, FRAT1, and β-catenin levels were assessed. After RNA-Seq, lncRNA expression profiles clearly distinguished RA patients from controls, and 190 upregulated lncRNAs and 131 downregulated lncRNAs were identified, which were mainly enriched in proliferative/immune/inflammatory pathways. Results of RT-qPCR showed that the levels of lncRNAs MTCO2P12, KCNQ5-IT1 and RP11-83J16.1 were increased, whereas lncRNAs LINC00570, RP11-342M1.6, and REXO1L4P were decreased in RA patients compared to controls. Notably, lncRNA RP11-83J16.1 correlated with increased inflammation and disease activity in RA patients. Additionally, lncRNA RP11-83J16.1 promoted cell proliferation, migration, invasion and inflammation, reduced apoptosis, and positively regulates cellular URI1, FRAT1 and β-catenin expression in RA-FLS. Rescue experiments revealed that URI1 overexpression compensated for the regulatory effects of lncRNA RP11-83J16.1 knockdown in RA-FLS. In conclusion, lncRNA RP11-83J16.1, a novel lncRNA identified by RNA-Seq, correlates with increased risk and disease activity of RA, and promotes RA-FLS proliferation, migration, invasion and inflammation by regulating URI1 and downstream β-catenin pathway components.