Long non-coding RNA SNHG1 regulates rheumatoid synovial invasion and proliferation by interaction with PTBP1.

Fibroblast-like synoviocytes (FLSs) in rheumatoid arthritis (RA) present proliferative and aggressive cell phenotype. RA-FLSs are the essential effector cells that lead to symptoms like synovial inflammation and joint destruction. Currently, the cause of RA-FLSs involving in the pathological process of RA remains unknown. Accumulate researches have demonstrated that lncRNAs may play a critical role in regulating the biological behaviors of RA-FLSs, but the mechanism is still unclear. Here, we found that lncRNA small nucleolar RNA host gene 1 (SNHG1) is up-regulated in RA-FLSs compared with FLSs from trauma arthritis and osteoarthritis patients. The results suggest that SNHG1 in RA-FLSs helps to sustain the cellular functions of proliferation, migration and invasion. Furthermore, the regulation mechanism depends on the interaction between SNHG1 and polypyridine tract-binding protein 1 (PTBP1). This interaction influences PTBP1 expression that participates in the regulation of RA-FLSs biological behaviors. Our results suggest that up-regulated SNHG1 of RA-FLSs may contribute to synovial aggression and disease progression in RA and be favourable for RA treatment target RA-FLSs. Copyright © 2020 Elsevier B.V. All rights reserved.

Citation

Fang Liu, Xiao-Xue Feng, Shang-Ling Zhu, Lang Lin, Hong-Yu Huang, Bai-Yu Zhang, Jian-Lin Huang. Long non-coding RNA SNHG1 regulates rheumatoid synovial invasion and proliferation by interaction with PTBP1. International immunopharmacology. 2021 Jan;90:107182

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PMID: 33218941

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