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A graphene-based nanocarrier modified with death receptor 4 (DR4) antibody and AKT siRNA has been developed, which can synergistically strengthen death receptor-mediated apoptosis and enhance the cancer therapeutic effect in vivo.
In contrast to apoptosis, necroptotic signaling was activated similarly by both DR4- or DR5-specific ligands..Our study provides the first systematic insight into DR4-/DR5-specific signaling in colorectal and pancreatic cancer cells
We found that pharmacological application of Golgi stress leads to induction of death receptors (DRs) 4 and 5. DR4 appears to be primarily responsible for the initiation of cell death downstream of Golgi stress, whereas DR5 seems to be more important for cell death triggered by endoplasmic reticulum (ER) stress in specific cancer cell lines
our results demonstrated that nanovectorization of TRAIL with BNNTs enhanced its binding to both DR4 and DR5 receptors at 37 degrees C. Our novel nanovector could potentially be used for delivering TRAIL to cells for cancer treatment
Apoptosis induced by TRAIL is preferentially induced by TRAIL-R1 pathway in breast/lung tumor cells.
By downregulating TRAIL-R1, TGFbeta1 may not only promote tumor escape from immune surveillance but also negatively impact on TRAIL- or TRAIL-R1-based therapy regimens for treatment of Pancreatic ductal adenocarcinoma.
Results show that downregulation of DR4 and DR5 by SLC26A2 confers resistance to TRAIL.
BAY61-3606 sensitizes colon cancer cells to TRAIL-induced apoptosis by up-regulating DR4 expression in p53-dependent manner and inhibiting NF-kappaB activity.
findings together highlight a previously undiscovered mechanism that positively regulates DR4 expression through activation of the MEK/ERK/AP-1 signaling pathway.
results suggest that the altered TRAIL, DR4 alleles and sTRAIL levels may be associated with some other potential biomarkers for vitiligo
The nanovectorization of TRAIL enhanced its binding to both DR4 and DR5 receptors at 37 degrees C and could potentially sensitized cancer cells to TRAIL induced apoptosis through simultaneous activation of DR4 and DR5 as described in this paper for the non-small lung carcinoma cell line (H1703), the two hepatocarcinoma cell lines (SK-Hep1, HUH) and the colon carcinoma cell line (HCT116WT).
Pro-survival effects by NF-kappaB, Akt and ERK(1/2) and anti-apoptosis actions by Six1 disrupt apoptotic functions of TRAIL-Dr4/5 pathway in ovarian cancer, which may explain why up-regulated DR4 and DR5 in ovarian cancer are associated with poor prognosis and low survival ratio of the patients.
Bee venom inhibits colon cancer cell growth, and these anti-proliferative effects may be related to the induction of apoptosis by activation of DR4 and DR5 and inhibition of NF-kappaB activity.
study involving a relatively large sample size showed that TNFRSF10 eQTL SNPs within lncRNAs might influence both hepatocellular carcinoma development and HBV infection
Study investigated the association between colorectal cancer and polymorphisms in TRAIL and DR4 gene in Pakistani patients; TRAIL gene 1595 C>T genotypes percentage in colorectal cancer patients was statistically non-significant; for DR4 A1322G, homozygous GG genotype was 36% in the patients and in controls: there was statistically insignificant difference (p> 0.05).
These statistical data suggest that Thr209Arg in exon 4 of the TRAIL-R1 gene may not represent a modifier of susceptibility to cancer.
TRAIL genetic polymorphisms do not contribute, but DR4 polymorphisms may contribute to susceptibility to head and neck cancer in Pakistani population.
The structure of death receptor 4 (DR4) in complex with TNF-related apoptosis-inducing ligand (TRAIL) has been determined at 3 A resolution and compared with those of previously determined DR5-TRAIL complexes.
LOC389641 promotes pancreatic ductal adenocarcinoma progression and increases cell invasion by regulating E-cadherin with the possible involvement of TNFRSF10A.
Results showed DR4 promotor methylation and low protein expression level in patients with lung squamous carcinoma which correlated with the prognosis of the disease.
The protein encoded by this gene is a member of the TNF-receptor superfamily. This receptor is activated by tumor necrosis factor-related apoptosis inducing ligand (TNFSF10/TRAIL), and thus transduces cell death signal and induces cell apoptosis. Studies with FADD-deficient mice suggested that FADD, a death domain containing adaptor protein, is required for the apoptosis mediated by this protein.
TNF-related apoptosis-inducing ligand receptor 1
, TRAIL receptor 1
, cytotoxic TRAIL receptor
, death receptor 4
, tumor necrosis factor receptor superfamily member 10A
, tumor necrosis factor receptor superfamily member 10a variant 2