WOFAPS 2025 8th World Congress of Pediatric Surgery

Heng Guo, Qiang Huang, Bin Yang

The Second Affiliated Hospital of Xi'an Jiaotong University

TRIM29, an oncogenic regulator in multiple malignancies, remains uncharacterized in infantile hemangioma (IH). This study investigated TRIM29's functional role and mechanistic basis in IH pathogenesis and treatment resistance. We observed significant TRIM29 upregulation in clinical IH specimens (*n* = 3) and cultured IH cell lines vs. controls. Using lentiviral-mediated TRIM29 knockdown and overexpression models, we demonstrated that TRIM29: Promotes IH cell proliferation and migration (*p* < 0.05), Suppresses apoptosis (*p* < 0.05), Activates STAT3/HIF-1α/VEGF signaling. In vivo, TRIM29 knockdown markedly inhibited subcutaneous tumor growth in nude mice (tumor volume reduction: 67.1%; *p* < 0.05). Mechanistically, TRIM29 interacts with STAT3 to induce non-proteolytic ubiquitination, sustaining STAT3 phosphorylation and downstream signaling. Crucially, propranolol (PR) exerted concentration-dependent anti-proliferative effects on IH cells. However, TRIM29 overexpression abolished PR-mediated growth inhibition (*p* < 0.05 vs. vector controls), indicating TRIM29-driven therapeutic resistance.