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

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. Examination of effects of TRIM24 knockdown or EGFRvIII on differential gene expression in glioma cells.

表皮生长因子受体（epidermal growth factor receptor, EGFR）的异常扩增与突变是胶质母细胞瘤（glioblastoma, GBM）中最常见的致癌事件，但其驱动肿瘤侵袭性发病的具体分子机制尚未完全明确。本研究发现，结合非经典组蛋白特征乙酰化H3赖氨酸23（non-canonical histone signature acetylated H3 lysine 23, H3K23ac）的含三联基序蛋白24（tripartite motif-containing 24, TRIM24）在胶质母细胞瘤临床标本中表达上调，且其是EGFR介导的肿瘤发生所必需的。本研究检测了敲低TRIM24或表达EGFRvIII对胶质瘤细胞基因表达差异的影响。