CEBPD (CCAAT/enhancer-binding protein delta) is a bZIP (basic leucine zipper) transcription factor that plays a crucial role in regulating cellular processes such as inflammation, cell growth, and apoptosis. It is induced by Toll-like receptor 4 (TLR4) signaling and is essential for the expression of many lipopolysaccharide (LPS)-induced genes, contributing to the clearance of bacterial infections. CEBPD functions as a tumor suppressor by inducing growth arrest and apoptosis in cancer cells, and its expression is often reduced in various cancers due to site-specific methylation. In glioblastoma, CEBPD acts as a master transcription factor controlling hypoxia-regulated genes and promotes tumor invasion through the ECM-integrin-mediated EGFR/PI3K pathway. Specifically, it activates the EGFR/PI3K/AKT pathway by directly binding to and regulating the expression of key ECM proteins such as fibronectin (FN1), which enhances the invasive capacity of cancer cells under hypoxic conditions. This highlights CEBPD as a potential therapeutic target in cancers with hypoxic microenvironments.
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