Long noncoding RNA LINC01615 promotes keloid development via sponging miR-590-3p to regulate FGF2 expression

Abstract

Background A keloid is a benign human skin tumor that resulted by fibrous overgrowths during wound healing. Long noncoding RNAs (lncRNAs) are indicated to involve in the development of keloid. However, the role of lncRNA LINC01615 in regulating keloid development and the underlying mechanism are still unknown. Methods The expression levels of LINC01615, miR-590-3p and fibroblast growth factor 2 (FGF2) mRNA were detected by quantitative real-time polymerase chain reaction (qRT-PCR). The protein levels of apoptosis-related proteins, α-smooth muscle actin (α-SMA), collagens and FGF2 were measured by western blot. The effect of LINC01615 on keloid development was assessed by cell proliferation, apoptosis and collagen deposition of keloid fibroblasts which were determined by Cell Counting Kit-8 (CCK-8), flow cytometry assay and the protein levels of collagens, respectively. The relationships between LINC01615 and miR-590-3p, miR-590-3p and FGF2 were predicated by online software and confirmed by dual-luciferase reporter assay and RNA pull-down assay. Results We first found that LINC01615 was upregulated in keloid tissues and fibroblasts, and LINC01615 promoted cell proliferation and collagen deposition and suppressed apoptosis in keloid fibroblasts. LINC01615 targeted miR-590-3p and downregulated miR-590-3p expression, and overexpression of miR-590-3p inhibited the development of keloid. Then, FGF2 was identified as a target of miR-590-3p. LINC01615 facilitated keloid development via regulating FGF2 expression through miR-590-3p. Conclusion Our study demonstrated that LINC01615 contributed to keloid development via the miR-590-3p/FGF2 axis.