ArticleOncogene2002
Low glucose-enhanced TRAIL cytotoxicity is mediated through the ceramide-Akt-FLIP pathway.
Article in Oncogene, 2002. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 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.
The trial behind it
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
29 citing papers in PubMed, 70 citations in OpenAlex.
- DZ-1-artesunate conjugate induces mitochondria-mediated, reactive oxygen species-dependent apoptosis in colorectal cancer tumoroids.Frontiers in pharmacology · 2026Article
- Current Advances in Anticancer Properties of Heptamethine Carbocyanine DZ-1 Conjugated to Artesunate: Generation of Reactive Oxygen Species.Journal of cellular biochemistry · 2025Article
- DZ-1-Artesunate Induces Apoptosis Via a Bid-, Bax-, and Bak-Independent Caspase-3 Activation Pathway.Journal of oncology research and therapy · 2025Article
- Glucose deprivation-induced endoplasmic reticulum stress response plays a pivotal role in enhancement of TRAIL cytotoxicity.Journal of cellular physiology · 2021Article
- Review
- Multiple Interactions Between Cancer Cells and the Tumor Microenvironment Modulate TRAIL Signaling: Implications for TRAIL Receptor Targeted Therapy.Frontiers in immunology · 2019Review
- Regulation of TNF-Related Apoptosis-Inducing Ligand Signaling by Glycosylation.International journal of molecular sciences · 2018Review
- Regulation of Tumor Progression by Programmed Necrosis.Oxidative medicine and cellular longevity · 2018Review
- Glucose Deprivation Induces ATF4-Mediated Apoptosis through TRAIL Death Receptors.Molecular and cellular biology · 2017Article
- Hyperglycemic Conditions Prime Cells for RIP1-dependent Necroptosis.The Journal of biological chemistry · 2016Article
- Marine Drugs Regulating Apoptosis Induced by Tumor Necrosis Factor-Related Apoptosis-Inducing Ligand (TRAIL).Marine drugs · 2015Review
- Trailing TRAIL Resistance: Novel Targets for TRAIL Sensitization in Cancer Cells.Frontiers in oncology · 2015Review
- Ceramide-orchestrated signalling in cancer cells.Nature reviews. Cancer · 2013Review
- Mitochondrial complex I inhibitors and forced oxidative phosphorylation synergize in inducing cancer cell death.International journal of cell biology · 2013Article
- Switching from aerobic glycolysis to oxidative phosphorylation modulates the sensitivity of mantle cell lymphoma cells to TRAIL.Oncogene · 2012Article
- Sugar-free approaches to cancer cell killing.Oncogene · 2011Review
- TRAIL sensitize MDR cells to MDR-related drugs by down-regulation of P-glycoprotein through inhibition of DNA-PKcs/Akt/GSK-3beta pathway and activation of caspases.Molecular cancer · 2010Article
- Article
- Article
- Pro-apoptotic Bid induces membrane perturbation by inserting selected lysolipids into the bilayer.The Biochemical journal · 2005Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
To examine whether the tumor microenvironment alters cytokine-induced cytotoxicity, human prostate adenocarcinoma DU-145 cells were exposed to tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) and/or glucose deprivation, a common characteristic of the tumor microenvironment. TRAIL alone reduced cell survival in a dose-dependent manner. Glucose deprivation alone induced no cytotoxicity within 4 h. However, the combination of TRAIL (50 ng/ml) and glucose deprivation for 4 h increased cell death and PARP cleavage by promoting activation of caspase-8 and caspase-3, relative to that of TRAIL alone. Similar results were observed in human colorectal carcinoma CX-1 cells. Data from immunoblotting analysis reveal that glucose deprivation-enhanced TRAIL cytotoxicity is inversely related to the intracellular level of FLICE inhibitory protein (FLIP) but not that of death receptor 5 (DR5). Results from mass spectrometry show that glucose deprivation elevates ceramide. The elevation of ceramide may cause dephosphorylation of Akt and maintain dephosphorylation of Akt in the presence of TRAIL and then subsequently down-regulate the expression of FLIP. Taken together, the present studies suggest that glucose deprivation enhances TRAIL-induced cytotoxicity through the ceramide-Akt-FLIP pathway.
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What OpenQuestion holds
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.