Lnc-H19 enhances anaerobic glycolysis of keloid fibroblasts by targeting the miR-214-5p/FGF2 axis.

Long non-coding RNA (lncRNA) H19 has been demonstrated as vital regulator in tumors. However, whether lnc-H19 mediated the development of keloid fibroblasts (KD) was unknown, this study was aimed to clarify the role and molecular mechanisms of lnc-H19 in KD. We have investigated the expression levels of lnc-H19, miR-214-5p and fibroblast growth factor 2 (FGF2) in KD skin samples and normal skin tissues as well as matched cells by real-time quantitative polymerase chain reaction (RT-qPCR) assay. The glycolysis ability of keloid fibroblasts was assessed by measuring glucose consumption, lactate production, and ATP level. The western blot assay was used to assay the expression levels of FGF2 and hexokinase 2 (HK2). Migration and invasion were analyzed by transwell in keloid fibroblasts. The bioinformatics database and dual-luciferase reporter assay were used to search and identify the target of miR-214-5p and lnc-H19. Lnc-H19 was overexpressed in KD tissues and keloid fibroblasts than normal skin tissues and normal fibroblasts, respectively. Small interfering RNA of lnc-H19 treatment markedly inhibited glycolysis, migration and invasion of keloid fibroblasts exposed to hypoxia, which was reserved by silencing of miR-214-5p or upregulation of FGF2. Mechanistically, lnc-H19 regulated KD development by regulation of miR-214-5p/FGF2 axis. In summary, lnc-H19 may exert regulatory functions in KD by targeting miR-214-5p/FGF2 axis, further regulated glycolysis, migration and invasion in keloid fibroblasts exposed to hypoxia, which might be a potential marker of KD diagnosis or progression.