TRIM24 is an oncogenic transcriptional co-activator of STAT3 in glioblastoma. Homo sapiens

Aberrant amplication and mutations of epidermal growth factor receptor (EGFR) are the most common oncogenic events in glioblastoma (GBM), but the mechanisms by which they promote aggressive pathogenesis are not well understood. Here, we determined that non-canonical histone signature acetylated H3 lysine 23 (H3K23ac)-binding protein tripartite motif-containing 24 (TRIM24) is upregulated in clinical specimens of glioblastoma and is required for EGFR-driven tumorigenesis. Overall design: Examination of effects of TRIM24 knockdown or EGFRvIII on differential gene expression in glioma cells.