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LERFS (long non-coding RNA negative regulator of fibroblast-like synoviocyte migration, SYNCRIP interacting) is a cytoplasmic lncRNA that is notably downregulated in fibroblast-like synoviocytes (FLS) from patients with rheumatoid arthritis (RA)[1]. In healthy FLS, LERFS binds to the RNA-binding protein SYNCRIP (hnRNP Q) to form a complex that suppresses the translation of mRNAs encoding RhoA, Rac1, and CDC42, which are critical small GTPases regulating cell motility and proliferation[1]. Decreased expression of LERFS in RA leads to increased translation of these targets, resulting in enhanced FLS migration, invasion, and proliferation, thereby contributing to synovial hyperplasia and joint destruction. Overexpression of LERFS in RA FLS reverses these pathogenic properties, making LERFS a proposed therapeutic target and a disease biomarker for RA-associated synoviocyte pathology[1][4].
Restoration of LERFS expression could decrease fibroblast-like synoviocyte (FLS) migration, invasion, and proliferation by reducing translation of RhoA, Rac1, and CDC42[1]
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