LncRNA FOXD2-AS1 promotes cell proliferation and invasion of fibroblast-like synoviocytes by regulation of miR-331-3p/PIAS3 pathway in rheumatoid arthritis. (4th July 2021)

• Record Type: Journal Article
• Authors: Zhao, Qirui; Zhao, Fengnian; Liu, Chang; Xu, Tongtong; Song, Keguan
• Is Part Of: Autoimmunity. Volume 54:Number 5(2021)
• Page Start: 254
• Page End: 263
• Publication Date: 2021-07-04
• Subjects: Fibroblast-like synoviocytes -- long non-coding RNA -- microRNA -- PIAS3 -- rheumatoid arthritis; Autoimmunity -- Periodicals; Autoimmune diseases -- Periodicals; 571.973
• DOI: 10.1080/08916934.2021.1919879
• Languages: English
• ISSNs: 0891-6934

Abstract

Abstract: Rheumatoid arthritis (RA) is a chronic autoimmune disorder that leads to systemic inflammation of diarthrodial joint, synovial hyperplasia, cartilage damage, and ultimately joint destruction and deformity. As the dominant non-immune cells in the synovium, fibroblast-like synoviocytes (FLSs) significantly contribute to the deterioration of RA. Our study aimed to explore the regulatory role of long non-coding RNA FOXD2-AS1 in RA progression. Compared to patients with joint trauma, the expression of FOXD2-AS1 was elevated in serum and synovial tissue samples of RA patients. FOXD2-AS1 knockdown inhibited the proliferation and invasion of rheumatoid FLSs but restored their apoptotic ability. Furthermore, FOXD2-AS1 acted as a sponge for microRNA (miR)-331-3p. The expressions of FOXD2-AS1 and miR-331-3p in synovial tissues of RA patients were negatively correlated. Protein inhibitor of activated STAT 3 (PIAS3) was predicted as a downstream target of miR-331-3p. The expressions of FOXD2-AS1 and PIAS3 in synovial tissues of RA patients were positively correlated, whereas a negative correlation was observed between the levels of miR-331-3p and PIAS3. Moreover, increased proliferation and invasion of rheumatoid FLSs induced by FOXD2-AS1 overexpression was inhibited by the knockdown of PIAS3. In summary, this study demonstrated that FOXD2-AS1 promoted RA progression via regulating the miR-331-3p/PIAS3 pathway, suggesting that therapeutic strategies based on the FOXD2-AS1/miR-331-3p/PIAS3 axis may represent a promising treatment approach for RA patients.