ArticleBiochimica et biophysica acta2012
DNA damage induces down-regulation of UDP-glucose ceramide glucosyltransferase, increases ceramide levels and triggers apoptosis in p53-deficient cancer cells.
Article in Biochimica et biophysica acta, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed, 18 citations in OpenAlex.
- Sphingolipid metabolism-related genes as diagnostic markers in pneumonia-induced sepsis: the AUG model.Scientific reports · 2025Article
- Insulin-inducible THRSP maintains mitochondrial function and regulates sphingolipid metabolism in human adipocytes.Molecular medicine (Cambridge, Mass.) · 2022Article
- The Role of Glycosyltransferases in Colorectal Cancer.International journal of molecular sciences · 2021Review
- Ceramide Metabolism Balance, a Multifaceted Factor in Critical Steps of Breast Cancer Development.International journal of molecular sciences · 2018Review
- The UDP-glucose ceramide glycosyltransferase (UGCG) and the link to multidrug resistance protein 1 (MDR1).BMC cancer · 2018Review
- Biological Roles of Aberrantly Expressed Glycosphingolipids and Related Enzymes in Human Cancer Development and Progression.Frontiers in physiology · 2018Review
- Alkaline ceramidase 2 and its bioactive product sphingosine are novel regulators of the DNA damage response.Oncotarget · 2016Article
- Changes in the metabolism of sphingolipids after subarachnoid hemorrhage.Journal of neuroscience research · 2015Article
- DNA promoter hypermethylation contributes to down-regulation of galactocerebrosidase gene in lung and head and neck cancers.International journal of clinical and experimental pathology · 2015Article
- Synergistic enhancement of cancer therapy using a combination of ceramide and docetaxel.International journal of molecular sciences · 2014Article
- p53 and Ceramide as Collaborators in the Stress Response.International journal of molecular sciences · 2013Article
Corrections and comments
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Authors and funding
6 authors at 3 institutions in 2 countries.
Funding
Abstract
DNA damaging agents typically induce an apoptotic cascade in which p53 plays a central role. However, absence of a p53-mediated response does not necessarily abrogate programmed cell death, due to the existence of p53-independent apoptotic pathways, such as those mediated by the pro-apoptotic molecule ceramide. We compared ceramide levels before and after DNA damage in human osteosarcoma (U2OS) and colon cancer (HCT116) cells that were either expressing or deficient in p53. When treated with mitomycin C, p53-deficient cells, but not p53-expressing cells, showed a marked increase in ceramide levels. Microarray analysis of genes involved in ceramide metabolism identified acid ceramidase (ASAH1, up-regulated), ceramide glucosyltransferase (UGCG, down-regulated), and galactosylceramidase (GALC, up-regulated) as the three genes most affected. Experiments employing pharmacological and siRNA agents revealed that inhibition of UGCG is sufficient to increase ceramide levels and induce cell death. When inhibition of UGCG and treatment with mitomycin C were combined, p53-deficient, but not p53-expressing cells, showed a significant increase in cell death, suggesting that the regulation of sphingolipid metabolism could be used to sensitize cells to chemotherapeutic drugs.
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