ArticleThe Journal of biological chemistry2012
Proteasome inhibition can impair caspase-8 activation upon submaximal stimulation of apoptotic tumor necrosis factor-related apoptosis inducing ligand (TRAIL) signaling.
Article in The Journal of biological chemistry, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
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Who cites it
21 citing papers in PubMed, 40 citations in OpenAlex.
- Review
- Reverse hierarchical DED assembly in the cFLIP-procaspase-8 and cFLIP-procaspase-8-FADD complexes.Nature communications · 2024Article
- Deciphering DED assembly mechanisms in FADD-procaspase-8-cFLIP complexes regulating apoptosis.Nature communications · 2024Article
- Proteasome inhibition triggers the formation of TRAIL receptor 2 platforms for caspase-8 activation that accumulate in the cytosol.Cell death and differentiation · 2022Article
- Advances in Studies on the Pharmacological Activities of Fucoxanthin.Marine drugs · 2020Review
- Function and mechanisms of microRNA-20a in colorectal cancer.Experimental and therapeutic medicine · 2020Review
- Fucoxanthin and Tumor Necrosis Factor-Related Apoptosis-Inducing Ligand (TRAIL) Synergistically Promotes Apoptosis of Human Cervical Cancer Cells by Targeting PI3K/Akt/NF-κB Signaling Pathway.Medical science monitor : international medical journal of experimental and clinical research · 2018Article
- Knockdown of miR-27a sensitizes colorectal cancer stem cells to TRAIL by promoting the formation of Apaf-1-caspase-9 complex.Oncotarget · 2017Article
- MiR-106b inhibitors sensitize TRAIL-induced apoptosis in hepatocellular carcinoma through increase of death receptor 4.Oncotarget · 2017Article
- Predicting the cell death responsiveness and sensitization of glioma cells to TRAIL and temozolomide.Oncotarget · 2016Article
- Enhanced efficacy against cervical carcinomas through polymeric micelles physically incorporating the proteasome inhibitor MG132.Cancer science · 2016Article
- MicroRNA-223 Increases the Sensitivity of Triple-Negative Breast Cancer Stem Cells to TRAIL-Induced Apoptosis by Targeting HAX-1.PloS one · 2016Article
- 2-DG-Regulated RIP and c-FLIP Effect on Liver Cancer Cell Apoptosis Induced by TRAIL.Medical science monitor : international medical journal of experimental and clinical research · 2015Article
- Fractional killing arises from cell-to-cell variability in overcoming a caspase activity threshold.Molecular systems biology · 2015Article
- Protective effect of RIP and c-FLIP in preventing liver cancer cell apoptosis induced by TRAIL.International journal of clinical and experimental pathology · 2015Article
- Modeling dynamics of cell-to-cell variability in TRAIL-induced apoptosis explains fractional killing and predicts reversible resistance.PLoS computational biology · 2014Article
- Systems biology of death receptor networks: live and let die.Cell death & disease · 2014Review
- Harnessing system models of cell death signalling for cytotoxic chemotherapy: towards personalised medicine approaches?Journal of molecular medicine (Berlin, Germany) · 2014Review
- Modulation of apoptosis sensitivity through the interplay with autophagic and proteasomal degradation pathways.Cell death & disease · 2014Review
- Modulating cell-to-cell variability and sensitivity to death ligands by co-drugging.Physical biology · 2013Article
Corrections and comments
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Authors and funding
8 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Tumor necrosis factor-related apoptosis inducing ligand (TRAIL) can induce extrinsic apoptosis, resulting in caspase-8 activation, but may also initiate transcription-dependent prosurvival signaling. Proteasome inhibitors were suggested to promote TRAIL signal transduction through the death-inducing signaling complex (DISC) by modulating the relative abundance of core DISC components, thereby enhancing caspase-8 activation and apoptosis. To test this hypothesis, we quantified the changes in DISC protein levels as an early consequence of proteasome inhibition in HeLa cervical cancer cells and, based on these data, mathematically modeled the proapoptotic TRAIL signaling toward caspase-8 activation. Modeling results surprisingly suggested that caspase-8 activation might be delayed in presence of proteasome inhibitors, in particular at submaximal TRAIL doses. Subsequent FRET-based single cell time-lapse imaging at conditions where transcription dependent prosurvival signaling was blocked confirmed this hypothesis: caspase-8 activity was delayed by hours in the presence of proteasome inhibitors epoxomicin or bortezomib. Corresponding delays were detected for effector caspase processing and cell death. Contrary to current models, we therefore provide evidence that synergies between TRAIL and proteasome inhibitors do not result from changes in the levels of core DISC signaling proteins.
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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.