IGF2BP2 Promotes Oral Squamous Cell Carcinoma Progression and Is Associated with MAPK Signaling and Macrophage-Related Immune Features

Insulin-like growth factor 2 mRNA-binding protein 2 (IGF2BP2) is an mRNA-binding protein implicated in tumorigenesis across multiple cancer types, but its functional role in oral squamous cell carcinoma (OSCC) remains incompletely understood. In this study, we combined bioinformatic analyses, validation in clinical specimens and cell lines, and functional experiments to investigate the role of IGF2BP2 in OSCC. IGF2BP2 was significantly elevated in OSCC and associated with poor overall survival. This upregulation was further validated in patient tissues and OSCC cell lines by quantitative real-time PCR, Western blot, and immunohistochemistry. IGF2BP2 knockdown markedly suppressed OSCC cell proliferation and migration in vitro and inhibited tumor growth in xenograft models in vivo. In parallel, IGF2BP2 depletion resulted in reduced phosphorylation of ERK and p38, supporting an association between IGF2BP2 and MAPK signaling activity in OSCC. In addition, immune-related pathway enrichment and immune infiltration analyses further suggested links between IGF2BP2 and the OSCC tumor immune microenvironment. Flow cytometric analysis of xenograft tumors revealed that IGF2BP2 knockdown altered macrophage-related immune features, including a reduced proportion of CD86+ M1-like tumor-associated macrophages. Collectively, these findings support an oncogenic role for IGF2BP2 in OSCC and suggest that IGF2BP2 is associated with MAPK signaling and macrophage-related immune features in OSCC.