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High levels of TRAIL-R3 and CCR-2 expression in tumor epithelial cells identified patients with early breast cancer with poor outcomes.
Results identified epigenetic inactivation of TNFRSF10C and TNFRSF10D in majority of cervical cancer cases.
DcRs regulate TRAIL sensitivity at a supracellular level
DcR1 levels in serum sample which were significantly lower in AMD patients.
DcR1 upregulation mediates temozolomide resistance.
membrane expression more common in endometrioid endometrial cancer than in normal endometrium
The membrane expression of the TRAIL receptors DR4, DR5, DcR1 and DcR2 is greater in normal endometrium than endometrioid adenocarcinoma (EAC). The level of the receptors in EAC is not dependent on grading and staging and does not predict survival.
the results presented here claim for a relevant impact of aberrant methylation of decoy receptors in melanoma and allow to understand how the silencing of DcR1 and DcR2 is related to melanomagenesis.
GATA4 and DcR1 promoter hypermethylation is tumor specific event in glioblastoma but they promoter methylation cannot be considered as a prognostic marker of glioblastoma survival.
Primary EOC is associated to a lower TRAIL-R3 expression.
Data show that about 20% of AML patients highly expressed decoy receptor TRAIL-R3, which was strongly correlated to a shortened overall survival.
Decoy receptors DcR1 and DcR2 on CD8+ T cells, but not on CD4-positive T cells, are positively correlated with patients' DAS scores.
Results suggest that DcR1 expression occurs in a subset of endometrial carcinomas and may contribute to resistance to TRAIL-induced apoptosis.
TNF-related apoptosis-inducing ligand (TRAIL) is not constitutively expressed in the human brain, whereas both apoptosis-mediating and apoptosis-blocking TRAIL receptors are found on neurons, astrocytes, and oligodendrocytes
analysis of the transcription initiation sites and promoter structure of the TRAIL-R3 gene
Cytotoxicity and apoptosis induced by TRAIL to beta-cell lines CM were inhibited competitively by soluble TRAIL receptors, R1, R2, R3 or R4.
likely to be involved in chronic pancreatitis; pancreatic stellate cells may directly contribute to acinar regression by inducing apoptosis of parenchymal cells in a TRAIL-dependent manner
cloned and characterized a p53 consensus element located within the first intron of the TRAIL-R3 gene
Our results demonstrate that DcR1 and DcR2 genes are frequently methylated in various tumor types, and aberrant methylation was the cause for silencing of DcR1 and DcR2 expression.
The DcR1 had no death domain and was anchored to the membrane via a glycophosphatidyl inositol tail.
The protein encoded by this gene is a member of the TNF-receptor superfamily. This receptor contains an extracellular TRAIL-binding domain and a transmembrane domain, but no cytoplasmic death domain. This receptor is not capable of inducing apoptosis, and is thought to function as an antagonistic receptor that protects cells from TRAIL-induced apoptosis. This gene was found to be a p53-regulated DNA damage-inducible gene. The expression of this gene was detected in many normal tissues but not in most cancer cell lines, which may explain the specific sensitivity of cancer cells to the apoptosis-inducing activity of TRAIL.
TNF-related apoptosis-inducing ligand receptor 3
, antagonist decoy receptor for TRAIL/Apo-2L
, cytotoxic TRAIL receptor-3
, decoy TRAIL receptor without death domain
, decoy receptor 1
, lymphocyte inhibitor of TRAIL
, tumor necrosis factor receptor superfamily member 10C
, tumor necrosis factor receptor superfamily, member 10c, decoy without an intracellular domain