ArticleCancer biology & therapy2010
Inhibition of NADPH oxidase by glucosylceramide confers chemoresistance.
Article in Cancer biology & therapy, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 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
20 citing papers in PubMed, 29 citations in OpenAlex.
- Sphingolipid biosynthesis is essential for metabolic rewiring during TScience advances · 2024Article
- The Role of Ceramide and Sphingolipid Metabolism in Cancer Therapeutics.Journal of oncology research and therapy · 2024Article
- Multiomic screening of invasive GBM cells reveals targetable transsulfuration pathway alterations.The Journal of clinical investigation · 2023Article
- Article
- Glycolipid Metabolite β-Glucosylceramide Is a Neutrophil Extracellular Trap-Inducing Ligand of Mincle Released during Bacterial Infection and Inflammation.Journal of immunology (Baltimore, Md. : 1950) · 2022Article
- Sphingolipids and Lymphomas: A Double-Edged Sword.Cancers · 2022Review
- Role of Sphingolipids in Multiple Myeloma Progression, Drug Resistance, and Their Potential as Therapeutic Targets.Frontiers in oncology · 2022Review
- Sphingolipids as Regulators of Neuro-Inflammation and NADPH Oxidase 2.Neuromolecular medicine · 2021Review
- Review
- Membrane Sphingolipids Regulate the Fitness and Antifungal Protein Susceptibility ofFrontiers in microbiology · 2019Article
- How Very-Long-Chain Fatty Acids Could Signal Stressful Conditions in Plants?Frontiers in plant science · 2016Article
- Redox Control of Multidrug Resistance and Its Possible Modulation by Antioxidants.Oxidative medicine and cellular longevity · 2016Review
- Dietary glucosylceramides suppress tumor growth in a mouse xenograft model of head and neck squamous cell carcinoma by the inhibition of angiogenesis through an increase in ceramide.International journal of clinical oncology · 2015Article
- {2-[1-(3-Methoxycarbonylmethyl-1H-indol-2-yl)-1-methyl-ethyl]-1H-indol-3-yl}-acetic Acid Methyl Ester Inhibited Hepatocellular Carcinoma Growth in Bel-7402 Cells and Its Resistant Variants by Activation of NOX4 and SIRT3.BioMed research international · 2015Article
- Evolving concepts in cancer therapy through targeting sphingolipid metabolism.Biochimica et biophysica acta · 2014Review
- NADPH oxidase biology and the regulation of tyrosine kinase receptor signaling and cancer drug cytotoxicity.International journal of molecular sciences · 2013Article
- Gaucher's disease and cancer: a sphingolipid perspective.Critical reviews in oncogenesis · 2013Review
- Ceramide kinase regulates TNFα-stimulated NADPH oxidase activity and eicosanoid biosynthesis in neuroblastoma cells.Cellular signalling · 2012Article
- A nonpolar blueberry fraction blunts NADPH oxidase activation in neuronal cells exposed to tumor necrosis factor-α.Oxidative medicine and cellular longevity · 2012Article
- Combinatorial therapies improve the therapeutic efficacy of nanoliposomal ceramide for pancreatic cancer.Cancer biology & therapy · 2011Article
Corrections and comments
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Authors and funding
9 authors at 3 institutions in 1 country.
Funding
Abstract
The bioactive sphingolipid ceramide induces oxidative stress by disrupting mitochondrial function and stimulating NADPH oxidase (NOX) activity, both implicated in cell death mechanisms. Many anticancer chemotherapeutics (anthracyclines, Vinca alkaloids, paclitaxel, and fenretinide), as well as physiological stimuli such as tumor necrosis factor α (TNFα), stimulate ceramide accumulation and increase oxidative stress in malignant cells. Consequently, ceramide metabolism in malignant cells and, in particular the up-regulation of glucosylceramide synthase (GCS), has gained considerable interest in contributing to chemoresistance. We hypothesized that increases in GCS activity and thus glucosylceramide, the product of GCS activity, represents an important resistance mechanism in glioblastoma. In our study, we determined that increased GCS activity effectively blocked reactive oxygen species formation by NOX. We further showed, in both glioblastoma and neuroblastoma cells that glucosylceramide directly interfered with NOX assembly, hence delineating a direct resistance mechanism. Collectively, our findings indicated that pharmacological or molecular targeting of GCS, using non-toxic nanoliposome delivery systems, successfully augmented NOX activity, and improved the efficacy of known chemotherapeutic agents.
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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.