ReviewCell death and differentiation2013
Non-canonical kinase signaling by the death ligand TRAIL in cancer cells: discord in the death receptor family.
Review in Cell death and differentiation, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 109 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
109 citing papers in PubMed, 173 citations in OpenAlex.
- TRAIL splice variant TRAILshort disrupts T cell receptor signaling and promotes immune tolerance in vivo.The Journal of clinical investigation · 2026Article
- 5-Aminoimidazole-4-carboxamide riboside, an AMPK activator, enhances TRAIL-mediated apoptosis in human bladder cancer cells in a p38 MAPK-dependent manner.Genes & genomics · 2026Article
- Article
- Jurkat T-Cell Antigen-Independent Elimination of PMA-Activated Neuroblastoma Cells Is Triggered by CCL2/CCR2, Depends Upon Lipid Raft LFA1/ICAM1 Immune Synapses, Is Mediated by m-TRAIL and Is Augmented by the TrkAIII Oncoprotein.International journal of molecular sciences · 2026Article
- Synthetic essentiality of TRAIL/TNFSF10 in VHL-deficient renal cell carcinoma.bioRxiv : the preprint server for biology · 2025Article
- Differential molecular mechanisms of bortezomib sensitization to rhTRAIL in non-small cell lung cancer cell lines.Exploration of targeted anti-tumor therapy · 2025Article
- Turn TRAIL Into Better Anticancer Therapeutic Through TRAIL Fusion Proteins.Cancer medicine · 2025Review
- TRAIL C1595T Variant Critically Alters the Level of sTRAIL in Terms of Histopathological Parameters in Colorectal Cancer.Indian journal of clinical biochemistry : IJCB · 2024Article
- The emerging role and mechanism of HMGA2 in breast cancer.Journal of cancer research and clinical oncology · 2024Review
- Review
- Death receptor 5 is required for intestinal stem cell activity during intestinal epithelial renewal at homoeostasis.Cell death & disease · 2024Article
- Small molecule activators of TAK1 promotes its activity-dependent ubiquitination and TRAIL-mediated tumor cell death.Proceedings of the National Academy of Sciences of the United States of America · 2023Article
- Article
- Breast tumors interfere with endothelial TRAIL at the premetastatic niche to promote cancer cell seeding.Science advances · 2023Article
- Article
- Harnessing TRAIL-induced cell death for cancer therapy: a long walk with thrilling discoveries.Cell death and differentiation · 2023Review
- 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.Frontiers in immunology · 2023Article
- TRAIL and its receptors in cardiac diseases.Frontiers in physiology · 2023Review
- Differential gene expression of immunity and inflammation genes in colorectal cancer using targeted RNA sequencing.Frontiers in oncology · 2023Article
- Synergistic activity of ABT-263 and ONC201/TIC10 against solid tumor cell lines is associated with suppression of anti-apoptotic Mcl-1, BAG3, pAkt, and upregulation of pro-apoptotic Noxa and Bax cleavage during apoptosis.American journal of cancer research · 2023Article
49 more citing papers are in PubMed but not listed here.
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Authors and funding
5 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Tumor necrosis factor-related apoptosis-inducing ligand (TRAIL)-based therapy is currently evaluated in clinical studies as a tumor cell selective pro-apoptotic approach. However, besides activating canonical caspase-dependent apoptosis by binding to TRAIL-specific death receptors, the TRAIL ligand can activate non-canonical cell survival or proliferation pathways in resistant tumor cells through the same death receptors, which is counterproductive for therapy. Even more, recent studies indicate metastases-promoting activity of TRAIL. In this review, the remarkable dichotomy in TRAIL signaling is highlighted. An overview of the currently known mechanisms involved in non-canonical TRAIL signaling and the subsequent activation of various kinases is provided. These kinases include RIP1, IκB/ NF-κB, MAPK p38, JNK, ERK1/2, MAP3K TAK1, PKC, PI3K/Akt and Src. The functional consequences of their activation, often being stimulation of tumor cell survival and in some cases enhancement of their invasive behavior, are discussed. Interestingly, the non-canonical responses triggered by TRAIL in resistant tumor cells resemble that of TRAIL-induced signals in non-transformed cells. Better knowledge of the mechanism underlying the dichotomy in TRAIL receptor signaling may provide markers for selecting patients who will likely benefit from TRAIL-based therapy and could provide a rationalized basis for combination therapies with TRAIL death receptor-targeting drugs.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.