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HuR-associated fibroblast migratory lncRNA (HAFML) is a long noncoding RNA (lncRNA) located on chromosome 4, implicated in the aggressive behavior of fibroblast-like synoviocytes within rheumatoid arthritis. HAFML is expressed at abnormally high levels in the synovial tissue of RA patients and promotes migration and invasion of FLSs by directly binding to HuR (ELAVL1), a key RNA-binding protein that stabilizes mRNAs. The HAFML–HuR complex enhances the stability and expression of the APPL2 mRNA, which contributes to cellular migration. Knockdown of HAFML or interference with HuR/APPL2 disrupts this pathway, suggesting therapeutic potential for targeting this lncRNA to control synovial aggression and joint destruction in rheumatoid arthritis. HAFML represents a novel molecular target class (lncRNA) distinct from protein-coding targets (e.g., receptors, enzymes) and may offer new therapeutic avenues for diseases characterized by fibroblast dysregulation.
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