Hemangioma (HA) is the most common benign vascular neoplasm of infancy that is resulted from abnormal proliferation of endothelial cells. Recent studies demonstrated that long non-coding RNAs (lncRNAs) were closely related to the pathogenesis of HA. LncRNA Nuclear enriched abundant transcript 1 (NEAT1) was involved in multiple tumor formation and biological behaviors of endothelial cells. However, the role and molecular mechanism of NEAT1 in HA are still unknown. The expression levels of NEAT1 and miR-361-5p were detected in proliferating phase HAs, involuting phase HAs, and normal skin tissues. The role and mechanism of NEAT1 on the proliferation, migration and apoptosis of hemangioma endothelial cells (HemECs) were analyzed by Cell Counting Kit (CCK)-8, transwell, flow cytometry, caspase-3 activity, dual-luciferase assay, RNA immunoprecipitation, Biotin-labeled miR-361-5p pulldown assay and western blot by gain- and loss-of-functions. We found that compared with normal skin tissues, NEAT1 expression was elevated, whereas miR-361-5p decreased in HA tissues especially in proliferating phase HAs. Downregulation of NEAT1 significantly suppressed the viability, PCNA expression and migration, but increased apoptotic cell numbers and caspase-3 activity of HemECs. NEAT1 functioned as a competing endogenous RNA to regulate VEGFA expression via sponging miR-361-5p. Taken together, these findings indicate that NEAT1 promotes the proliferation and migration, whereas inhibits the apoptosis of HemECs via regulating miR-361-5p/VEGFA axis.
Keywords: Apoptosis; Hemangioma; Long non-coding RNA NEAT1; Migration; miR-361-5p/VEGFA.
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