The antiapoptotic decoy receptor TRID/TRAIL-R3 is a p53-regulated DNA damage-inducible gene that is overexpressed in primary tumors of the gastrointestinal tract

作者: M Saeed Sheikh , Ying Huang , Ester A Fernandez-Salas , Wafik S El-Deiry , Helmut Friess

DOI: 10.1038/SJ.ONC.1202763

关键词:

摘要: Both DR4 and DR5 have recently been identified as membrane death receptors that are activated by their ligand TRAIL to engage the intracellular apoptotic machinery. TRID (also named TRAIL-R3) is an antagonist decoy receptor lacks cytoplasmic domain. protects from TRAIL-induced apoptosis competing with for binding TRAIL. has shown be overexpressed in normal human tissues but not malignantly transformed cell lines. a p53-regulated gene we reported expression induced response genotoxic stress both p53-dependent independent manner (Sheikh et al., 1998). In current study, demonstrate also agents ionizing radiation methyl methanesulfonate (MMS) predominantly p53 wild-type cells, whereas UV-irradiation does induce expression. Consistent these results, exogenous upregulates of endogenous p53-null cells. Thus, appears target regulated manner. Using primary gastrointestinal tract (GIT) tumors matching tissue, first time enhanced GIT. It is, therefore, possible overexpressing GIT may gain selective growth advantage escaping apoptosis.

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