IGF2BP3 promotes infantile hemangioma progression and is associated with VEGFA signaling

N6-methyladenosine (m6A) modification plays a crucial role in tumorigenesis. As an m6A “reader,” insulin-like growth factor II mRNA-binding protein 3 (IGF2BP3) is implicated in various cancers, but its function in infantile hemangioma (IH) remains unclear. This study aimed to investigate the expression and biological role of IGF2BP3 in IH pathogenesis. Bioinformatics analysis was performed using the GSE127487 dataset. Hemangioma-derived endothelial cells (HemECs) were isolated from proliferating IH tissues, with human umbilical vein endothelial cells (HUVECs) as controls. IGF2BP3 expression was assessed in IH tissues and cells via immunohistochemistry (IHC) and Western blot. IGF2BP3 was knocked down in HemECs using sh-IGF2BP3, with negative control shRNA (sh-NC) as a control. Subsequently, cell proliferation, migration and invasion, and apoptosis were evaluated. The mRNA and protein levels of IGF2BP3 and vascular endothelial growth factor A (VEGFA) were measured by quantitative real-time polymerase chain reaction (qRT-PCR) and Western blot. IHC showed that IGF2BP3 expression was significantly higher in proliferative stage compared to involution stage ( P < 0.001). IGF2BP3 mRNA and protein were also elevated in HemECs versus HUVECs ( P < 0.001). Knockdown of IGF2BP3 significantly suppressed HemECs proliferation (CCK-8 at 72 h, P < 0.001), colony formation (323 ± 15.28 vs. 376 ± 17.90, P < 0.05), migration (40.67 ± 9.07 vs. 216 ± 29.20, P < 0.001), and invasion ( P < 0.001), while promoting apoptosis (4.49% ± 0.15% vs. 2.96% ± 0.27%, P < 0.001). Furthermore, IGF2BP3 silencing led to a significant reduction in VEGFA mRNA and protein levels ( P < 0.05). IGF2BP3 is overexpressed in proliferative stage IH and promotes the aggressive phenotypes of HemECs, and its effects are associated with VEGFA expression. Those findings suggest that IGF2BP3 may serve as a novel therapeutic target for IH.