• TRAIL triggers apoptosis upon engagement of one of its two agonistic receptors, named DR4 (death receptor 4) (33) and DR5 (death receptor 5) (7, 46). (opioid-receptors.com)
  • In response to TRAIL, these receptors recruit the adaptor protein FADD (Fas-associated death domain), through death domain homophilic interactions (5), and the initiators procaspase-8 and -10, through death effector domain interactions with FADD, hence forming the macromolecular complex called DISC (death-inducing signaling complex). (opioid-receptors.com)
  • In addition to the agonistic TRAIL receptors DR4 and DR5, TRAIL can bind to related but antagonistic receptors, including TRID or TRAIL-R3 (11, 27, 32) and TRUNDD or TRAIL-R4 (10), also coined DcR1 (decoy receptor 1) and DcR2 (decoy receptor 2), respectively. (opioid-receptors.com)
  • Transient overexpression of DcR1 or DcR2 in TRAIL-sensitive Sav1 tumor cells prevents cell death triggering by TRAIL (10, 11), and recent evidence indicates that tumor and normal cells can acquire resistance to TRAIL-induced killing by up-regulating TRAIL antagonistic receptors (6, 8, 9, 34). (opioid-receptors.com)
  • Here, we review tumor-NK cell interactions, discuss the mechanisms by which NK cells generate an antitumor immune response, and discuss NK cell-based therapeutic strategies targeting activating, inhibitory, and co-stimulatory receptors. (frontiersin.org)
  • In a second project we are investigating the induction of apoptosis by activation of death receptors for the ligand TRAIL in breast and ovarian cancer cells. (cancer.gov)
  • We have shown that most breast and ovarian cancer cell lines are resistant to the induction of apoptosis by TRAIL, the ligand for the death receptors DR4 and DR5. (cancer.gov)
  • Breast cancer tumors that do not express hormone receptors or have amplification of Her2/Neu (so called triple-negative tumors) have a poor prognosis and no validated molecular targets. (cancer.gov)
  • Here, we developed TRAIL-functionalized liposomes (LipoTRAIL, LT) to mimic membrane-displayed TRAIL for efficient activation of death receptors DR4 and DR5 and enhanced induction of apoptosis, which were combined with an anti-EGFR single-chain Fv fragment (scFv) for targeted delivery to EGFR-positive tumor cells. (uni-stuttgart.de)
  • Tumor necrosis factor (TNF)-related apoptosis-inducing ligand (TRAIL) binds to death receptors and induces apoptosis in various cancer cell lines while sparing normal cells. (oncotarget.com)
  • Shikonin derivatives cause apoptosis and cell cycle arrest in human chondrosarcoma cells via death receptors and MAPK regulation. (ebsco.com)
  • Background: TNF-related apoptosis-inducing ligand (TRAIL) is a member of the TNF superfamily that can either induce cell death or activate survival pathways after binding to death receptors (DRs) DR4 or DR5. (ebsco.com)
  • The apoptotic response of cells can be induced by the intrinsic and the extrinsic pathway, the former being mediated by the mitochondria and the latter activated by ligand stimulation of death receptors at the cell surface [ 1 ]. (biomedcentral.com)
  • In this study, we focussed on the gene expression of toll-like receptors (TLRs), chemokine receptors (CCRs) and death receptor ligands in SARS-CoV infected DCs. (biomedcentral.com)
  • Ligand binding to cognate receptors activates initiator caspases directly in a death-inducing signaling complex. (deathbase.org)
  • Objective: We aimed to investigate the signalling crosstalk of TNF-related apoptosis-inducing ligand, TRAIL death receptors, tumour protein p53, and programmed cell death (PDCD5) with IQGAPs. (waocp.org)
  • Also, we targeted the crosstalk between IQGAPs genes with decoy receptors, nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB), and interleukins -8 (IL-8) and its receptor genes in a designed model of hepatocellular carcinoma induced in male Balb/c mice. (waocp.org)
  • Apoptosis can be triggered by the engagement of cell surface receptors by their ligands. (ox.ac.uk)
  • A growing number of receptors belonging to the TNF receptor family have been identified that contain a conserved cytoplasmic death domain. (ox.ac.uk)
  • The latter two are receptors for the cytotoxic ligand TNF-related apoptosis-inducing ligand (TRAIL), and one of the paradoxes raised by the cloning of these molecules was why do most cells not die upon contact with the widely expressed TRAIL molecule? (ox.ac.uk)
  • Mechanisms of peripheral tolerance include inactivation of autoantigen-recognizing T and B cells by the induction of apoptosis, anergy or conversion into immunosuppressive regulatory cells. (frontiersin.org)
  • 2) We investigate induction of apoptosis in breast cancer cells by TRAIL receptor agonists. (cancer.gov)
  • Thus, we established a multifunctional liposomal TRAIL formulation (ILT) with improved pharmacokinetic and pharmacodynamic behavior, characterized by targeted delivery and increased induction of apoptosis due to multivalent TRAIL presentation. (uni-stuttgart.de)
  • TNF superfamily member (TRAIL) is a type II transmembrane protein and is responsible for initiating apoptosis. (ekb.eg)
  • TRAIL (also known as Apo2 ligand), is a trimeric protein, a TNF superfamily member, expressed as a type-II transmembrane protein and plays a physiological role in anti-tumor immune surveillance [ 1 - 6 ]. (oncotarget.com)
  • member of the tumor necrosis factor superfamily known as TRAIL (tumor necrosis factor-related apoptosis-inducing ligand) (16). (opioid-receptors.com)
  • This gene encodes a member of the tumor necrosis factor (TNF) cytokine family which is a ligand for osteoprotegerin and functions as a key factor for osteoclast differentiation and activation. (nih.gov)
  • In the current study, we demonstrate that DcR1 and DcR2 inhibit TRAIL-induced apoptosis by distinct mechanisms. (opioid-receptors.com)
  • LIT is expressed predominantly on PBL, where it can competitively inhibit TRAIL-induced apoptosis through DR4/TRICK2, and may function to modulate lymphocyte sensitivity to TRAIL. (ox.ac.uk)
  • Fig. 2 The apoptotic effect of combined parthenolide (PT) and tumor necrosis factor (TNF)-related apoptosis-inducing ligand (TRAIL) treatment. (researchensemble.com)
  • The CD56 bright population produces immunoregulatory cytokines, including interferon-γ (IFN-γ), tumor necrosis factor-beta (TNF-B), tumor necrosis factor-α (TNF-α), granulocyte macrophage-colony stimulating factor (GMCSF), IL-10, and IL-13 ( 4 ). (frontiersin.org)
  • Circulating osteoprotegerin (OPG), a member of the receptor activator of nuclear factor kappa-B (RANK) axis, may influence breast cancer risk via its role as the decoy receptor for both the RANK ligand (RANKL) and tumor necrosis factor-related apoptosis-inducing ligand (TRAIL). (biomedcentral.com)
  • Bone homeostasis is maintained by the interplay between the receptor activator of nuclear factor kappa-B (RANK), its soluble activation ligand (RANKL), and OPG. (biomedcentral.com)
  • Other cytokines including tumour necrosis factor alpha, transforming growth factor beta 1, interleukin 1 and interleukin 6 have no inhibitory effect. (microbiologyresearch.org)
  • Among these associations, we found KIM-1 (kidney injury molecule-1), TNFR (TNF [tumor necrosis factor] receptor) 1 and 2, TRAIL-R2 (TRAIL [TNF-related apoptosis-inducing ligand] receptor 2), and RETN (resistin) to be associated with all 4 lipid fractions. (lu.se)
  • Apo-2L oder „tumor necrosis factor (TNF)-related apoptosis ligand" (TRAIL), TRAIL, ist ein Mitglied der TNF-Familie und ein vielversprechendes Protein für die Krebs. (uni-marburg.de)
  • Apo-2L or tumor necrosis factor (TNF)-related apoptosis ligand, TRAIL, is one of several members of the TNF family and due its selectivity towards transformed versus normal cells it bears the potential as a cancer therapeutic agent. (uni-marburg.de)
  • Jeffrey, I. W. , Bushell, M. , Tilleray, V. J. , Morley, S. and Clemens, M. J. (2002) Inhibition of protein synthesis in apoptosis: differential requirements by the tumor necrosis factor alpha family and a DNA-damaging agent for caspases and the double-stranded RNA-dependent protein kinase. (gla.ac.uk)
  • In MCF-7 breast cancer cells, tumor necrosis factor α (TNFα) and TNF-related apoptosis-inducing ligand inhibit overall translation by a mechanism that requires caspase (but not necessarily caspase-3) activity. (gla.ac.uk)
  • Tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) is known to cause apoptosis in several types of malignant tumor cells through its interaction with the death domain-containing receptor, death receptor 5 (DR5). (nih.gov)
  • Cytokines secreted by adipocytes, such as tumor necrosis factor-α, transforming growth factor-β, and interleukin-6, are implicated in NAFLD. (wjgnet.com)
  • Tumor necrosis factor-related apoptosis- inducing ligand polymorphism. (ekb.eg)
  • The impact of inflammatory cytokines tumour necrosis factor-α and transformation growth factor-β on this model, as well as other variables such as hypoxia and the anti-fibrosis drug Halofuginone were assessed. (edu.au)
  • Transcriptional profiling revealed a tumour necrosis factor-α mediated apoptotic response in organoids and an inflammatory response in both the organoids and hepatic stellate cells. (edu.au)
  • This protein was shown to activate antiapoptotic kinase AKT/PKB through a signaling complex involving SRC kinase and tumor necrosis factor receptor-associated factor (TRAF) 6, which indicated this protein may have a role in the regulation of cell apoptosis. (nih.gov)
  • The mammalian extrinsic apoptosis pathway is triggered by Fas ligand (FasL) and Apo2 ligand/tumor necrosis factor (TNF)-related apoptosis-inducing ligand (Apo2L/TRAIL). (deathbase.org)
  • At infection sites, activated T cells secrete cytokines (eg, interferon-gamma [IFN-gamma]) that induce production of macrophage migration inhibitory factor, preventing macrophages from leaving. (msdmanuals.com)
  • Polymorphisms for interleukin-4 (IL-4) -590 promoter, IL-4 intron3, and tumor necrosis factor alpha -308 promoter: non-association with endometriosis. (cdc.gov)
  • Tumor necrosis factor-alpha promotor polymorphisms and endometriosis. (cdc.gov)
  • The tumor necrosis factor-alpha promoter -1031C polymorphism is associated with decreased risk of endometriosis in a Japanese population. (cdc.gov)
  • Genetic contribution of tumor necrosis factor (TNF)-alpha gene promoter (-1031, -863 and -857) and TNF receptor 2 gene polymorphisms in endometriosis susceptibility. (cdc.gov)
  • Genetic variation in tumour necrosis factor and lymphotoxin is not associated with endometriosis in an Australian sample. (cdc.gov)
  • Association between susceptibility of endometriosis and the gene polymorphism of tumor necrosis factor]. (cdc.gov)
  • Association of tumor necrosis factor-{alpha} gene polymorphisms with advanced stage endometriosis. (cdc.gov)
  • Tumor necrosis factor (TNF)-TNF receptor gene polymorphisms and their serum levels in Korean women with endometriosis. (cdc.gov)
  • Association of the tumor necrosis factor-alpha -1031T/C and its combination with interleukin-6 -634C/G gene polymorphisms with susceptibility to endometriosis]. (cdc.gov)
  • Association between endometriosis and polymorphisms in tumor necrosis factor-related apoptosis-inducing ligand (TRAIL), TRAIL receptor and osteoprotegerin genes and their serum levels. (cdc.gov)
  • Although RT is an important modality for cancer treatment, the consequential changes caused by RT in the tumor microenvironment (TME) have not yet been fully elucidated. (nature.com)
  • Furthermore, inflammatory mediators released by irradiated dying cells can attract and regulate immune cells in the tumor microenvironment (TME), further killing cancer cells. (nature.com)
  • Emerging evidence indicates that lncRNAs participate in crosstalk between tumor and stroma, and reprogramming of tumor immune microenvironment (TIME). (biomedcentral.com)
  • Together, they form the microenvironment in which the tumor is located, namely tumor microenvironment (TME). (biomedcentral.com)
  • Among the components of TME, distinct populations of innate and adaptive immune cells consist of tumor immune microenvironment (TIME). (biomedcentral.com)
  • Synthesis and Evaluation of 177 Lu-DOTA-PD-L1-i and 225 Ac-HEHA-PD-L1-i as Potential Radiopharmaceuticals for Tumor Microenvironment-Targeted Radiotherapy. (ebsco.com)
  • Current cancer therapies focus on reducing immunosuppression and remodeling the tumor microenvironment to inhibit metastasis, cancer progression, and therapeutic resistance. (ebsco.com)
  • In accordance, attempts have been made to establish a link between the immune system and the tumor microenvironment, to comprehend tumor progression and achieve effective therapeutic approaches. (fortunejournals.com)
  • Immunotherapy mainly includes immune checkpoint inhibitors (ICIs), such as inhibitors of PD-1 (programmed cell death 1)/programmed cell death ligand 1 (PD-L1). (nature.com)
  • instead of targeting tumor cells, the goal of immunotherapy is to augment and expand the immune system's intrinsic antitumor response. (frontiersin.org)
  • TRAIL has gained considerable interest in oncology since it displays specific antitumoral activity against a wide range of tumor cells (14, 41, 47) without significant side effects, at least in mice and monkeys (3, 21, 22). (opioid-receptors.com)
  • Background/Aims Combination therapy utilizing tumor necrosis element (TNF)-related apoptosis-inducing ligand (TRAIL) together with other anticancer real estate agents is a promising technique to overcome TRAIL level of resistance in malignant cells. (researchensemble.com)
  • Mixture PT and Path treatment inhibited cell development and induced apoptosis of HT-29 cells significantly. (researchensemble.com)
  • Mouse monoclonal to PRAK that HT-29 cells are resistant to TRAIL-induced cell death highly. (researchensemble.com)
  • A) HT-29 and HCT 116 cells had been treated with Path every day and night in the concentrations indicated … To look for the synergistic aftereffect of PT on TRAIL-induced cell loss of life HT-29 cells had been incubated in the lack or existence of PT (10 μM) and Path (5 25 or 40 ng/mL). (researchensemble.com)
  • Co-treatment with TRAIL and 3-Butylidenephthalide PT caused a 3-fold increase in the proportion of annexin V-positive cells (41.86%) indicating that PT promotes TRAIL-induced apoptosis in TRAIL-resistant cells. (researchensemble.com)
  • After treatment with TRAIL and/or 5-fluorouracil (5-FU) … We also evaluated cell cycle modifications induced by PT and TRAIL in HT-29 cells. (researchensemble.com)
  • In combined treatment a much greater sub-G1 population (27.77%) was observed indicating that the combination of two agents dramatically promoted apoptosis in TRAIL-resistant cells (Fig. 2B). (researchensemble.com)
  • There is compelling clinical and experimental evidence to suggest that natural killer (NK) cells play a critical role in the recognition and eradication of tumors. (frontiersin.org)
  • However, as tumors progress, cancerous cells develop immunosuppressive mechanisms that circumvent NK cell-mediated killing, allowing for tumor escape and proliferation. (frontiersin.org)
  • Therapeutic intervention aims to reverse tumor-induced NK cell suppression and sustain NK cells' tumorlytic capacities. (frontiersin.org)
  • However, a class of important immune-modulators is conspicuously absent: agents that utilize the power of innate immune cells to eradicate tumors. (frontiersin.org)
  • First described in 1975, NK cells were initially identified as a distinct sub-population of lymphocytes by their capacity to spontaneously lyse tumor cells ( 1 ). (frontiersin.org)
  • NK cells are now accepted to play an important role in both the adaptive and innate immune responses that govern infection, autoimmunity, and tumor immunosurveillance ( 2 , 3 ). (frontiersin.org)
  • Cancer cells avoid apoptosis by a variety of genetic and epigenetic mechanisms. (cancer.gov)
  • Our goal is to selectively trigger apoptosis in the cancer cells. (cancer.gov)
  • We have demonstrated that resistance to TRAIL-induced apoptosis can be overcome by co-incubation of the cells with chemotherapeutic agents, semi-synthetic retinoids (such as 4HPR), or molecularly targeted agents (such as anti-ErbB-2 antibodies). (cancer.gov)
  • Our current work utilizes biochemical and genetic approaches to identify mechanisms that regulate the induction of death by TRAIL ligand in breast and ovarian cancer cells. (cancer.gov)
  • In our third project we are using functional genomic approaches and tumor genetics to identify new therapeutic targets in triple-negative breast cancer cells. (cancer.gov)
  • RT-induced damage to cancer cells leads to different outcomes, such as survival, senescence, or death. (nature.com)
  • In addition, tumor-associated antigens (TAAs) produced by irradiated tumor cells can be captured by antigen-presenting cells (APCs) in the TME and presented to T cells. (nature.com)
  • α -TOS is highly selective for malignant cells, inducing them into apoptotic death largely via the mitochondrial route. (nature.com)
  • More recent data show that OPG is also produced in breast tumor cells, and that it can promote tumor growth and metastasis [ 5 , 6 ]. (biomedcentral.com)
  • Cells induced to undergo apoptosis by treatment with recombinant human TRAIL gave a population of cells that was Annexin V-FITC positive (second panel, M2). (bdbiosciences.com)
  • A small number of Annexin-V positive cells in the untreated population represents a basal level of apoptosis (far left/first panel). (bdbiosciences.com)
  • The results indicate that clone RIK-2 can block cell mediated killing induced by recombinant human TRAIL as measured by Annexin V-FITC staining of Jurkat cells. (bdbiosciences.com)
  • The specific binding of the scFv-anti-TRAIL-R2 fragment to TRAIL-R2 expressing tumor cells was confirmed by FACS analysis. (uni-marburg.de)
  • Only minimal lytic activity of the scFv-anti-TRAIL-R2 fragment on a variety of tumor cells could be detected. (uni-marburg.de)
  • The anti-tumoral efficacy of IZ-TRAIL alone or in combination with different chemotherapeutic drugs was evaluated on a variety of tumor cells. (uni-marburg.de)
  • Besides the high apoptosis-inducing activity on cancer cells, no toxicity in mice and on freshly isolated human hepatocytes of either IZ-TRAIL alone or in combination with diverse chemotherapeutic drugs was observed. (uni-marburg.de)
  • Therefore, in contrast to non-tagged versions of TRAIL this recombinant IZ-TRAIL shows high activity against tumor cells and, at the same time, it is not toxic to primary cells. (uni-marburg.de)
  • In their review " Natural and Adaptive Immunity to Cancer ", Vesely and colleagues draw from recent mouse models of cancer and human clinical data to describe how cells, effector molecules, and pathways of the immune system act to suppress and control tumor cells. (massgenomics.org)
  • Alternatively, cells that sense injury or loss of mitochondrial integrity may undergo programmed cell death (apoptosis). (massgenomics.org)
  • The idea that the immune system might recognize and destroy tumor cells was conceived 50-100 years ago. (massgenomics.org)
  • Exposure of mammalian cells to agents that induce apoptosis results in a rapid and substantial inhibition of protein synthesis. (gla.ac.uk)
  • In addition to tumor cells, there are also important stromal components in tumor niche. (biomedcentral.com)
  • Natural killer (NK) cells were identified in the blood and lymphoid organs of humans and experimental animals as cells capable of killing tumors, virus-infected cells, and, in some instances, normal cells, in the absence of previous deliberate or known sensitization. (mhmedical.com)
  • 1 , 2 NK cells are now considered to belong to the cellular subgroup that is characterized by the production of interferon (IFN)- γ within the family of innate lymphoid cells (ILCs), a family of developmentally related cells involved in innate immunity and tissue development. (mhmedical.com)
  • In the present study, we showed that co-treatment with troglitazone (TGZ), a synthetic ligand of peroxisome proliferator-activated receptor γ (PPARγ), and TRAIL synergistically induced apoptosis through DR5 upregulation in human colon cancer DLD-1 cells. (nih.gov)
  • We investigated the effects of calmodulin(CaM) antagonists, trifluoperazine(TFP) and tamoxifen(TMX), on TRA-8-induced apoptosis and tumorigenesis of TRA-8-resistant pancreatic cancer cells, and underlying mechanisms. (oncotarget.com)
  • TFP or TMX alone did not induce apoptosis of resistant PANC-1 cells, while they dose-dependently enhanced TRA-8-induced apoptosis. (oncotarget.com)
  • Altogether, we have demonstrated that CaM antagonists enhance TRA-8-induced apoptosis of TRA-8-resistant pancreatic cancer cells by increasing DR5 expression and enhancing recruitment of apoptotic signal while decreasing survival signals in DR5-associated DISC. (oncotarget.com)
  • Dysregulation of apoptosis of tumor cells plays an important role in the pathogenesis of pancreatic cancer and their resistance to therapies [ 5 ]. (oncotarget.com)
  • ADI downregulates survivin, upregulates DR5 receptor and sensitizes cancer cells to TRAIL induced apoptosis. (oncotarget.com)
  • Many cancer cells are intrinsically resistant to TRAIL-induced apoptosis. (oncotarget.com)
  • MUC16 expression in EOC cells is associated with increased tumorigenesis and inhibiton of genotoxic drug-induced apoptosis. (biomedcentral.com)
  • We show that MUC16 attenuates apoptosis, activation of caspase-8 and mitochondria activation in EOC cells in response to TRAIL. (biomedcentral.com)
  • Down-regulation of cFLIP following treatment of MUC16-expressing OVCAR3 cells with cFLIP siRNA also increases TRAIL-induced apoptosis. (biomedcentral.com)
  • These findings indicate that MUC16 protects EOC cells against TRAIL-induced apoptosis through multiple mechanisms including the blockade of TRAIL R2 expression and the regulation of cFLIP expression at both the transcriptional and the protein level. (biomedcentral.com)
  • Apoptosis plays a critical role in cellular homeostasis and prevents the development of tumor cells. (biomedcentral.com)
  • Pro-caspase-8 activation can directly result in cleavage of caspase-3 to execute apoptosis (type I cells) or cleave Bid to produce a truncated form (tBid), which induces the release of cytochrome c from the mitochondria leading to caspase-9 and subsequent caspase-3 activation (type II cells) as it is the case for EOC cells. (biomedcentral.com)
  • Human mast cells induce osteoclastogenesis through cell surface RANKL. (nih.gov)
  • Ectopic expression of these ligands during embryogenesis induced apoptosis in erythroblasts and notochord cells. (deathbase.org)
  • In addition, this molecule was capable of transmitting apoptotic signals mediated through not only Fas but also the TNF receptor in mouse Casp8-deficient cells. (deathbase.org)
  • Recently, stem cells are being engineered to carry therapeutic reagents to target tumor sites. (bmrat.org)
  • This re- view discusses stem cell applications in transplantation, stem cell-based carriers, induced-pluripotent stem cells, can- cer stem cells, and potential of stem cells engineering to revolutionize cancer treatment. (bmrat.org)
  • These cells are called induced pluripotent stem cells (iPSCs). (bmrat.org)
  • Relevant information has now been established on solid tumors and their micro-environments, which include immune, endothelial and mesenchymal cells. (fortunejournals.com)
  • Basal cell carcinoma (BCC) is a nonmelanocytic skin cancer (ie, an epithelial tumor) that arises from basal cells (ie, small, round cells found in the lower layer of the epidermis). (medscape.com)
  • Apparently, certain immune system pathways (e.g. inflammation) instead serve to promote tumor growth. (massgenomics.org)
  • The binding of ligands to TLRs may trigger downstream signaling pathways that are involved in both the cytokine release during the primary induction of inflammation and secondary activation of anti-inflammatory mechanisms [ 12 ]. (biomedcentral.com)
  • These results suggest that combined treatment with TGZ and TRAIL may be promising as a new therapy against malignant tumors. (nih.gov)
  • Background: Although chondrosarcoma is the second most common primary malignant bone tumor, treatment options are limited due to its extensive resistance to a chemo- and radiation therapy. (ebsco.com)
  • 4 According to the number of tumor-infiltrating lymphocytes, tumors can be divided into three phenotypes: immune-inflamed, immune-excluded, and immune-desert types. (nature.com)
  • Lymphocyte inhibitor of TRAIL (TNF-related apoptosis-inducing ligand): a new receptor protecting lymphocytes from the death ligand TRAIL. (ox.ac.uk)
  • In this Commentary, we discuss the implications of these findings for the regulation of apoptosis by Bcl-2 family proteins. (biologists.com)
  • In this study, we investigated the associations between proteins related to CVD and triglyceride (TG), total cholesterol, LDL (low-density lipoprotein), and HDL (high-density lipoprotein) cholesterol levels in individuals from the general population. (lu.se)
  • Further, 15 proteins were related to both TG and HDL cholesterol in a consistent and biologically expected manner, that is, higher TG and lower HDL cholesterol or vice versa. (lu.se)
  • Numerous cellular proteins detect DNA damage and induce senescence , a permanent change of state characterized by morphological and gene expression changes. (massgenomics.org)
  • Thus, therapeutics that induce, restore, and maintain immune tolerance toward these autoantigens represent the "Holy Grail" of treatments for autoimmune diseases. (frontiersin.org)
  • Immune-inflamed tumors are called hot tumors, while the latter two are collectively referred to as cold tumors, and they respond poorly to immunotherapy. (nature.com)
  • The primary objectives of this study are: - To determine the proportion of children with Severe Acute Respiratory Syndrome Coronavirus 2 (SARS-CoV-2) related death, rehospitalization or major complications after infection with SARS-CoV-2 and/or Multisystem Inflammatory Syndrome in Children (MIS-C), and - To determine immunologic mechanisms and immune signatures associated with disease spectrum and subsequent clinical course during the year of follow-up. (stanford.edu)
  • However, in certain cell types, the extrinsic pathway also induces mitochondrial damage by cleaving the pro-apoptotic Bcl-2 family protein Bid to its activated truncated form (tBid), which leads to Bak and Bax activation. (biologists.com)
  • Delineation of the cell-extrinsic apoptosis pathway in the zebrafish. (deathbase.org)
  • Thus, the extrinsic apoptosis pathway in zebrafish closely resembles its mammalian counterpart and cooperates with the intrinsic pathway to trigger tissue-specific apoptosis during embryogenesis in response to ectopic Apo2L/TRAIL expression. (deathbase.org)
  • There can, however, be few similarities between the two, as the bone marrow is a common site of metastasis of solid tumors too [6]. (fortunejournals.com)
  • Selective inhibitors of nuclear export block pancreatic cancer cell proliferation and reduce tumor growth in mice. (karmanos.org)
  • Similar experiments with embryonic fibroblasts from control mice and animals defective for expression of the double-stranded RNA-regulated protein kinase (PKR) reveal requirements for both caspase activity and PKR for inhibition of protein synthesis in response to TNFα. (gla.ac.uk)
  • Targeted disruption of the related gene in mice led to severe osteopetrosis and a lack of osteoclasts. (nih.gov)
  • The complexity of the human bone marrow, with context to haematological malignancies, is more difficult to elucidate with the present strategies compared to the niche of solid tumors. (fortunejournals.com)
  • To date, the molecular mechanisms by which DcR1 and DcR2 confer resistance to TRAIL-induced apoptosis remain unclear (1, 6, 9, 13). (opioid-receptors.com)
  • However, anti-TNF-α therapies have limitations, including known adverse safety risk, loss of therapeutic efficacy due to drug resistance, and lack of efficacy in numerous autoimmune diseases, including multiple sclerosis. (frontiersin.org)
  • Furthermore, the TRAIL system seems to circumvent the resistance of tumors induced by treatment with chemo- and radiotherapie. (uni-marburg.de)
  • However, clinical success has been limited due to poor PK and development of resistance to death receptor-induced apoptosis. (oncotarget.com)
  • It can also behave as a tumour suppressor gene. (wikipedia.org)
  • Our results demonstrates that SARS-CoV did not modulate TLR-1 to TLR-10 gene expression but significantly induced the expression of CCR-1, CCR-3, and CCR-5. (biomedcentral.com)
  • There was also strong induction of TNF-related apoptosis-inducing ligand (TRAIL), but not Fas ligand gene expression in SARS-CoV infected DCs. (biomedcentral.com)
  • T cell activation was reported to induce expression of this gene and lead to an increase of osteoclastogenesis and bone loss. (nih.gov)
  • Association of tumor necrosis factors-beta gene polymorphism with endometriosis in women in Guangdong Province]. (cdc.gov)
  • Effect of gene polymorphism of TNF-beta on the concentration of TNF in serum of patient with endometriosis]. (cdc.gov)
  • Compared to that of the soluble TRAIL, the plasma half-life of the functionalized liposomes was strongly extended, and increased antitumor activity of LT and ILT was demonstrated in a xenograft tumor model. (uni-stuttgart.de)
  • RÉSUMÉ L'objectif de l'étude était d'évaler l'importance clinique du ligand de CD40 soluble (sCD40L) chez des patients atteints d'un carcinome hépatocellulaire (CHC) associé au virus de l'hépatite C (VHC). (who.int)
  • Unfortunately, even among those patients who undergo resection for pancreatic cancer and have tumor-free margins, the 5-year survival rate after resection is 10% to 25% [ 3 ]. (oncotarget.com)
  • Knockdown of CASP5 greatly inhibited GBM proliferation and resulted in G1 cell cycle arrest along with higher apoptosis ratios in vitro and in vivo, while overexpression led to the opposite phenomenon. (cancerindex.org)
  • Tumor necrosis element (TNF)-related apoptosis-inducing ligand (TRAIL) is a member of the TNF family that induces cancer cell death by apoptosis with some selectivity. (opioid-receptors.com)
  • 2 PT Enhances TRAIL - induced Apoptotic Cell Death To support the earlier observations annexin-V analysis was performed using FACScan. (researchensemble.com)
  • A) Apoptotic cell death induced by combination treatment. (researchensemble.com)
  • Analysis of TRA-8-induced death-inducing-signaling-complex (DISC) identified recruitment of survival signals, CaM/Src, into DR5-associated DISC, which was inhibited by TMX/TFP. (oncotarget.com)
  • TRAIL induces apoptosis after binding to death receptor 4 (DR4 or TRAIL-R1) and/or death receptor 5 (DR5 or TRAIL-R2) [ 1 , 2 , 4 - 7 ]. (oncotarget.com)
  • MUC16 decreases TRAIL receptor R2 (DR5) expression and inhibits pro-caspase-8 activation at the death-inducing signaling complex (DISC). (biomedcentral.com)
  • These include Fas, TNF-R1, lymphocyte-associated receptor of death (LARD), DR4, and TNF-related apoptosis-inducing ligand receptor inducer of cell killing-2 (TRICK2). (ox.ac.uk)
  • the micrornas (mirnas or mirs), a type of small non-coding rna , have emerged as molecular regulators that can have key roles as tumor suppressors or oncogenes in pathogenesis and progression of different malignancies, including breast cancer. (icbcongress.com)
  • An aberrant miRNA expression could contribute to cancer development and progression [ 6 , 7 ] and could affect their target genes that are involved in many biological processes, such as cell differentiation, proliferation, apoptosis, metabolism, and development [ 8 ]. (hindawi.com)
  • 3 PT enhances TRAIL-induced Apoptotic Via Caspase Activation Many anticancer agencies can handle initiating caspase activation and inducing. (researchensemble.com)
  • Upon TRAIL binding, DcR1 and DcR2 fail to recruit FADD and, consequently, fail to induce downstream cell signaling events leading to apoptosis (10, 32). (opioid-receptors.com)
  • Interestingly, the SARS-CoV infected DCs showed low expression of antiviral cytokines (IFN-α, IFN-β, IFN-γ and IL-12p40), moderate upregulation of proinflammatory cytokines (TNF-α and IL-6) but significant upregulation of inflammatory chemokines (macrophage inflammatory protein (MIP)-1α/CCL3, regulated upon activation, normal T cell expressed and secreted (RANTES)/CCL-5, interferon-inducible protein of 10 kD (IP-10)/CXCL10 and monocyte chemotactic protein (MCP)-1/CCL2. (biomedcentral.com)
  • The upregulation of chemokines and CCRs may facilitate DC migration from the infection site to the lymph nodes, whereas the increase of TRAIL may induce lymphocyte apoptosis. (biomedcentral.com)
  • The antitumor effect provided by natural killing has been observed in tumors of hematopoietic and non-hematopoietic origins and reported in diverse in vivo models and clinical series ( 8 ). (frontiersin.org)
  • These therapies inhibit the proinflammatory action of TNF-α in common autoimmune diseases such as rheumatoid arthritis, psoriasis, ulcerative colitis, and Crohn's disease. (frontiersin.org)
  • TRAIL promotes the polarization of human macrophages toward a proinflammatory M1 phenotype and is associated with increased survival in cancer patients with high tumor macrophage content. (ebsco.com)
  • NK cell infiltration into tumor tissue is associated with better disease prognosis in colorectal cancer, clear cell renal cell carcinoma, and lung carcinomas ( 9 - 11 ). (frontiersin.org)
  • This study observed reduced breast cancer risk among women with comparatively high OPG concentrations, but given a small number of incident cases ( n = 76), risk by tumor subtypes (e.g., by estrogen (ER) and progesterone (PR) receptor status) was not investigated. (biomedcentral.com)
  • Breast cancer tumor specimens and their matched non-cancerous tissues were obtained from 30 patients diagnosed with breast cancer. (icbcongress.com)
  • The World Health Organization reported that cancer is one of the major causes of disease-related deaths before the age of 70 [2]. (fortunejournals.com)
  • Globally, cancer incidences and mortality is alarming and can often be co-related with the socio-economic development of a given population. (fortunejournals.com)
  • Overexpression of the active form of this enzyme induces apoptosis in fibroblasts. (cancerindex.org)
  • Alcohol also interferes with proper inflammatory responses by disturbing the enzymatic processing of TNFα by TNFα Converting Enzyme (TACE) and abrogating TNFα/TACE function [ 11 , 12 ]. (cdc.gov)