Research Status of Death Domain-associated Protein

Abstract

Overexpression of death domain-associated protein (DAXX) is a common feature of many cancers, and it structurally has binding sites for many interactors (eg, ARTX, HDAC3). According to functional studies, DAXX interacts with a number of DNA-binding transcription factors (TFs), epigenetic regulators, core histones, and proteins involved in chromatin to induce apoptosis via the extrinsic death receptor pathway. Functions as a co-activator or transcriptional inhibitor of cobalt diplus to regulate gene expression. Current studies have found that DAXX is expressed upregulated in ovarian cancer. Additionally, research has demonstrated that DAXX increases the tumorigenicity of prostate cancer by preventing autophagy pathways. In contrast, patients with pancreatic neuroendocrine tumors have lower survival rates when their DAXX is lost. A powerful breast tumor-initiating cell (TIC) inhibitor, DAXX also inhibits the production of pluripotent and EMT genes via promoters that may bind to pluripotent TIC-related genes. As a result, DAXX has powerful carcinogenic properties and potential new therapeutic targets. This article will introduce the protein from the aspects of DAXX's structure, function, and relationship with cancer.