ArticleOncogene2008
Ionizing radiation modulates the TRAIL death-inducing signaling complex, allowing bypass of the mitochondrial apoptosis pathway.
Article in Oncogene, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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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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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
14 citing papers in PubMed, 44 citations in OpenAlex.
- Apoptosis as a Potential Target to Arrest and Survival of Hydatid Cyst.Advanced biomedical research · 2023Article
- Enhancing radiation response by a second-generation TRAIL receptor agonist using a new in vitro organoid model system.Clinical and translational radiation oncology · 2020Article
- Effects of retinoic acid-inducible gene-I-like receptors activations and ionizing radiation cotreatment on cytotoxicity against human non-small cell lung cancerOncology letters · 2018Article
- Combination treatment of TRAIL, DFMO and radiation for malignant glioma cells.Journal of neuro-oncology · 2015Article
- PicoGreen assay of circular DNA for radiation biodosimetry.Radiation research · 2015Article
- Stress-induced changes in gene interactions in human cells.Nucleic acids research · 2014Article
- Polyubiquitination and proteasomal turnover controls the anti-apoptotic activity of Bcl-B.Oncogene · 2013Article
- Ubiquitination by the membrane-associated RING-CH-8 (MARCH-8) ligase controls steady-state cell surface expression of tumor necrosis factor-related apoptosis inducing ligand (TRAIL) receptor 1.The Journal of biological chemistry · 2013Article
- The role of TRADD in TRAIL-induced apoptosis and signaling.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2011Article
- Strategizing the clone wars: pharmacological control of cellular sensitivity to radiation.Molecular interventions · 2010Review
- HLJ1 is a novel caspase-3 substrate and its expression enhances UV-induced apoptosis in non-small cell lung carcinoma.Nucleic acids research · 2010Article
- Control of death receptor ligand activity by posttranslational modifications.Cellular and molecular life sciences : CMLS · 2010Review
- REG I enhances chemo- and radiosensitivity in squamous cell esophageal cancer cells.Cancer science · 2008Article
- Enhancement of glioma radiotherapy and chemotherapy response with targeted antibody therapy against death receptor 5.International journal of radiation oncology, biology, physics · 2008Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors at 4 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
In many tumor cell types, ionizing radiation (IR) or DNA-damaging anticancer drugs enhance sensitivity to tumor necrosis factor-related apoptosis-inducing ligand (TRAIL)-induced apoptosis, which is of great clinical interest. We have investigated the molecular mechanism underlying the response to combined modality treatment in p53-mutant Jurkat T leukemic cells overexpressing Bcl-2. These cells are largely resistant to individual treatment with TRAIL or IR, but sensitive to combined treatment, in vitro as well as in vivo. We demonstrate that IR and DNA-damaging anticancer drugs enable TRAIL receptor-2 and CD95/Fas to bypass the mitochondrial pathway for effector caspase activation. This was validated by RNA interference for Bax and Bak and by overexpression of dominant-negative Caspase-9. Improved effector caspase activation was neither caused by altered expression of proapoptotic components nor by impaired activity of inhibitor of apoptosis proteins or nuclear factor-kappaB signaling. Rather, we found that pretreatment of cells with IR caused quantitative and qualitative changes in death receptor signaling. It strongly improved the capacity of ligand-bound receptors to recruit FADD and activate Caspase-8 and -10 in the death-inducing signaling complex, while c-FLIP(L) levels were unaffected.
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Registered trials
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.