AI Article Synopsis
- - Heparin binding epidermal growth factor-like growth factor (HB-EGF) plays a role in both normal bodily processes and the development of chronic diseases, particularly cancer.
- - Its expression is influenced by various transcription factors, including AP-1, NF-κB, and microRNAs, which may work together to create an autocrine loop that amplifies HB-EGF signals.
- - Recent research suggests that targeting HB-EGF could be a promising strategy for treating cancer and atherosclerosis, as this review explores the connection between HB-EGF and its regulatory factors.
Article Abstract
Heparin binding epidermal growth factor-like growth factor (HB-EGF) is involved in development and homeostasis as well as in pathological processing of chronic diseases, especially cancer. Enhancement of HB-EGF expression is directly or indirectly regulated by transcriptional factors, including activator protein-1 (AP-1), specificity protein (SP)1, SP3, nuclear factor kappa B (NF-κB), hypoxia inducible factor 1, alpha subunit (HIF-1α, myogenic differentiation 1 (MyoD), Wilms tumor 1 (WT-1) and snail homolog 1 (Snail), and also by microRNAs. These transcription or post-transcription factors may communicate to form an autocrine HB-EGF amplification loop. Emerging evidence has indicated that HB-EGF is a rational target for the therapy of cancer and atherosclerosis. In this review, we discuss the relationship between the HB-EGF autocrine loop and HB-EGF transcriptional factors, and we highlight HB-EGF as a therapeutic target in diverse diseases.
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