LncRNA is involved in the proliferation, migration, and invasion of rheumatoid fibroblast-like synoviocytes.

BACKGROUND

Fibroblast-like synoviocytes (FLSs), which can migrate and directly invade the cartilage and the bone, are crucial players in joint damage in rheumatoid arthritis (RA). Nevertheless, the detailed mechanisms underlying the aberrant activation of RA FLSs remain unclear. Several studies have attempted to explore the relationship between long non-coding RNAs (lncRNAs) and RA pathology; however, the role of lncRNAs in RA is unknown. The present study aimed to determine the functions of tumor necrosis factor-α and heterogeneous nuclear ribonucleoprotein L-related immunoregulatory lincRNA () in RA FLSs migration and invasion.

METHODS

Small interfering RNA targeting or lentivirus overexpressing was used to knockdown or overexpress . Quantitative reverse transcription polymerase chain reaction (PCR) was employed for the detection of RNA expression. The proliferation rate of RA FLSs was measured using a 5-ethynyl-2'-deoxyuridine (EdU) incorporation assay. Migration and invasion were detected using a transwell chamber. Downstream targets were identified using a human cell cycle real-time PCR array and a human cell motility real-time PCR array.

RESULTS

A significant decrease in expression was found in RA FLSs compared with cells from healthy control (HC)patients. is mainly localized in the nucleus. Knockdown of increased the proliferation, migration, and invasion of RA FLSs. In contrast, overexpression had the opposite effect. knockdown increased interleukin-1β (IL-1β)-triggered expression of matrix metalloproteinase ()-1, , and . overexpression led to a significant decrease in expression in response to stimulation with IL-1β. Furthermore, we observed that the expression levels of cyclin-dependent kinase 1 () and G2 and S phase-expressed-1 (), both of which are associated with cellular mobility and proliferation, were downregulated with overexpression.

CONCLUSIONS

Reduced expression of lncRNA represses the proliferation, migration, and invasion of RA FLSs, suggesting that lncRNA might be a potential target for RA therapy.