Silencing long non‑coding RNA NEAT1 suppresses the tumorigenesis of infantile hemangioma by competitively binding miR‑33a‑5p to stimulate HIF1α/NF‑κB pathway.

Infantile hemangioma (IH) is one of the most common vascular tumors that occurs during childhood, but its pathogenesis is currently not completely understood. Even though lncRNA nuclear paraspeckle assembly transcript 1 (NEAT1) plays vital roles in tumorigenesis of malignant tumors, its roles in IH remain unclear. Therefore, we evaluate the function of lncRNA NEAT1 in IH. Reverse transcription‑-quantitative PCR indicated that IH tissues exhibited high expression levels of NEAT1 and hypoxia‑inducible factor 1α (HIF1α), and low expression levels of the microRNA (miR)‑33a‑5p. Small interfering RNA‑mediated depletion of NEAT1 suppressed hemangioma endothelial cell (HemEC) proliferation, migration and invasion. The data suggested that NEAT1 positively regulated HIF1α expression by sponging miR‑33a‑5p in HemECs. miR‑33a‑5p overexpression or HIF1α silencing also acted to suppress HemEC proliferation, migration and invasion. Furthermore, the results indicated that the NEAT1/miR‑33a‑5p/HIF1α axis regulated the NF‑κB signaling pathway. Collectively, the results revealed that depletion of lncRNA NEAT1 suppressed the tumorigenesis of IH by competitively binding miR‑33a‑5p and thereby stimulating the HIF1α/NF‑κB signaling pathway.