LncRNA SNHG16 drives proliferation, migration, and invasion of hemangioma endothelial cell through modulation of miR-520d-3p/STAT3 axis.

It has been verified that long noncoding RNAs (lncRNAs) have great effects on various biological behaviors of human diseases. Although more and more lncRNAs have been studied in human cancers, countless lncRNAs still need to be excavated. This study aims to investigate the impacts of lncRNA SNHG16 on proliferation and metastasis of human hemangioma endothelial cell (HemECs). qRT-PCR analysis was carried out to explore the expression pattern of SNHG16, miR-520d-3p, and STAT3. The effect of SNHG16 on cell proliferation was detected by MTT and colony formation assay. Flow cytometry analysis was performed to test the apoptosis of HemECs cells. Migration and invasion of HemECs cells were determined and examined by transwell assays. Tube formation assay helped to observe the influence of SNHG16 expression on the vasoformation of HemECs cells. The correlations among SNHG16, miR-520d-3p, and STAT3 were certified by bioinformatics analysis, pull-down assay, and dual-luciferase reporter assay. Finally, rescue assays were conducted to demonstrate the effects of SNHG16-miR-520d-3p-STAT3 axis on biological behaviors of HemECs cell. SNHG16 was strongly expressed in proliferating phase hemangioma tissues and HemECs cells. Silenced SNHG16 negatively affected proliferation, migration, and invasion of HemECs cell. LncRNA SNHG16 acted as a ceRNA to upregulate STAT3 through binding with miR-520d-3p in HemECs cell. LncRNA SNHG16 acted as a ceRNA to drive proliferation, vasoformation, migration, and invasion of HemECs cells through modulating miR-520d-3p/STAT3 axis.