Keloid is a skin disease characterized by fibrous hyperplasia, which is often difficult to cure. Long non-coding RNAs (lncRNAs) have been shown to be associated with the development of many diseases. However, the role and mechanism of lncRNA H19 in keloid has been less studied. Our study found that lncRNA H19 expression was increased in keloid tissues and fibroblasts. Besides, H19 knockdown hindered the proliferation, migration, invasion, extracellular matrix (ECM) deposition, and enhanced the apoptosis of keloid fibroblasts. Further experiments showed that microRNA (miR)-769-5p could be sponged by H19, and its knockdown reversed the suppression effect of H19 knockdown on keloid formation. Eukaryotic initiation factor 3A (EIF3A) was found to be a target of miR-769-5p, and its overexpression inverted the inhibition effect of miR-769-5p overexpression on keloid formation. Moreover, the expression of EIF3A was regulated by H19 and miR-769-5p in keloid fibroblasts. Collectively, LncRNA H19 might play an active role in keloid formation, which might provide a new target for the treatment of keloid.
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