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• W2129305290 abstract "•TRAIL is able to induce apoptosis in a wide range of cancers. •TRAIL has been functionalized to diversify its traditional tumor-killing role. •Strategies to facilitate its deployment are discussed. •We provide a perspective for improving prospects of clinical implementation. Tumor necrosis factor (TNF)-related apoptosis-inducing ligand, or TRAIL, is a promising anticancer agent as it can induce apoptosis in a wide range of cancers whilst generally sparing non-malignant cells. However, the translation of TRAIL into the clinic has been confounded by its short half-life, inadequate delivery methods, and TRAIL-resistant cancer cell populations. In this review, we discuss how TRAIL has been functionalized to diversify its traditional tumor-killing role and novel strategies to facilitate its effective deployment in preclinical cancer models. The successes and failures of the most recent clinical trials using TRAIL agonists are highlighted and we provide a perspective for improving its clinical implementation. Tumor necrosis factor (TNF)-related apoptosis-inducing ligand, or TRAIL, is a promising anticancer agent as it can induce apoptosis in a wide range of cancers whilst generally sparing non-malignant cells. However, the translation of TRAIL into the clinic has been confounded by its short half-life, inadequate delivery methods, and TRAIL-resistant cancer cell populations. In this review, we discuss how TRAIL has been functionalized to diversify its traditional tumor-killing role and novel strategies to facilitate its effective deployment in preclinical cancer models. The successes and failures of the most recent clinical trials using TRAIL agonists are highlighted and we provide a perspective for improving its clinical implementation. a type of programmed cell death that leads to characteristic cellular changes and death. These events include blebbing, cell shrinkage, nuclear fragmentation, chromatin condensation, and chromosomal fragmentation. There are two apoptosis pathways: the extrinsic pathway acts independently of the transcription factor p53 and is mediated by death receptors such as the TNF receptor superfamily. The intrinsic pathway is triggered in response to cellular stress and DNA damage and involves activation of p53. or cysteine-aspartic proteases are a family of enzymes that are essential in apoptosis, necrosis, and inflammation. There are two types: initiator caspases cleave inactive proforms of effector caspases, therefore activating them. Effector caspases, once activated, cleave other protein substrates to trigger the apoptotic cascade. the use of more than one medication or therapy to treat a disease. a protein interaction module composed of six α-helices. DDs are found in the cytoplasmic tails of death receptors and mediate their self-association, which initiates apoptosis signal transduction events. a multiprotein complex including members of the apoptosis-inducing cellular receptors such as TRAIL-R1 and caspase-8. Upon ligand binding, the DISC transduces a signaling cascade resulting in apoptosis. trimeric cytokine receptors that bind to tumor necrosis factors and induce apoptosis. In contrast to the apoptosis-inducing death receptors, decoy receptors are unable to transduce an apoptotic signal. For example, TRAIL-R3 lacks a DD and TRAIL-R4 has a truncated DD enabling TRAIL to bind but rendering them unable to initiate apoptosis. the most common and aggressive malignant primary brain tumor in humans. leads to the release of pro-death factors from the mitochondrial intermembrane space, which engages caspases to propagate the apoptotic signaling cascade. an antibody fragment consisting of a single monomeric variable antibody domain. Nanobodies are able to bind to specific antigens and have a molecular weight of 12–15 kDa compared with the 150–160 kDa of conventional antibodies. a group of cytokines whose family can cause apoptosis. All members form trimeric complexes that are recognized by their cognate receptor. a cytokine that is produced and secreted by the majority of mammalian cells. TRAIL elicits apoptosis primarily in tumor cells by binding to death receptors expressed at the cell surface. cancer cells that are resistant to apoptosis induced by TRAIL. Resistance can be intrinsic (cells were always resistant to TRAIL) or acquired (cells that were once sensitive to TRAIL have become resistant after repeated exposure). Understanding the mechanisms underlying resistance and developing strategies to overcome it is vital for the successful use of TRAIL for cancer therapy." @default.
• W2129305290 created "2016-06-24" @default.
• W2129305290 creator A5034567480 @default.
• W2129305290 creator A5075841716 @default.
• W2129305290 date "2013-11-01" @default.
• W2129305290 modified "2023-10-07" @default.
• W2129305290 title "TRAIL on trial: preclinical advances in cancer therapy" @default.
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• W2129305290 doi "https://doi.org/10.1016/j.molmed.2013.08.007" @default.
• W2129305290 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/3880796" @default.
• W2129305290 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/24076237" @default.
• W2129305290 hasPublicationYear "2013" @default.
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