ArticleInternational journal of molecular sciences2014
Nuclear lipid microdomain as resting place of dexamethasone to impair cell proliferation.
Article in International journal of molecular sciences, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed, 18 citations in OpenAlex.
- Sphingomyelin regulates the transcriptional machinery in nuclear lipid microdomains.Communications biology · 2025Article
- Effect of Sphingomyelin and Vitamin D3 Intake on the Rabbit Brain.International journal of molecular sciences · 2025Article
- Nuclear Lipid Microdomains Regulate Daunorubicin Resistance in Hepatoma Cells.International journal of molecular sciences · 2018Article
- Effect of Vitamin D in HN9.10e Embryonic Hippocampal Cells and in Hippocampus from MPTP-Induced Parkinson's Disease Mouse Model.Frontiers in cellular neuroscience · 2018Article
- The Many Facets of Sphingolipids in the Specific Phases of Acute Inflammatory Response.Mediators of inflammation · 2018Review
- Radiation and Thyroid Cancer.International journal of molecular sciences · 2017Review
- Crosstalk between sphingolipids and vitamin D3: potential role in the nervous system.British journal of pharmacology · 2017Review
- Nuclear Lipids in the Nervous System: What they do in Health and Disease.Neurochemical research · 2017Review
- Acid sphingomyelinase as target of Lycium Chinense: promising new action for cell health.Lipids in health and disease · 2016Article
- Why high cholesterol levels help hematological malignancies: role of nuclear lipid microdomains.Lipids in health and disease · 2016Article
- Very-long-chain fatty acid sphingomyelin in nuclear lipid microdomains of hepatocytes and hepatoma cells: can the exchange from C24:0 to C16:0 affect signal proteins and vitamin D receptor?Molecular biology of the cell · 2015Article
- Gentamicin arrests cancer cell growth: the intriguing involvement of nuclear sphingomyelin metabolism.International journal of molecular sciences · 2015Article
Corrections and comments
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Authors and funding
14 authors at 5 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The action of dexamethasone is initiated by, and strictly dependent upon, the interaction of the drug with its receptor followed by its translocation into the nucleus where modulates gene expression. Where the drug localizes at the intranuclear level is not yet known. We aimed to study the localization of the drug in nuclear lipid microdomains rich in sphingomyelin content that anchor active chromatin and act as platform for transcription modulation. The study was performed in non-Hodgkin's T cell human lymphoblastic lymphoma (SUP-T1 cell line). We found that when dexamethasone enters into the nucleus it localizes in nuclear lipid microdomains where influences sphingomyelin metabolism. This is followed after 24 h by a cell cycle block accompanied by the up-regulation of cyclin-dependent kinase inhibitor 1A (CDKN1A), cyclin-dependent kinase inhibitor 1B (CDKN1B), growth arrest and DNA-damage 45A (GADD45A), and glyceraldehyde 3-phosphate dehydrogenase (GAPDH) genes and by the reduction of signal transducer and activator of transcription 3 (STAT3) and phospho signal transducer and activator of transcription 3 (phoshoSTAT3) proteins. After 48 h some cells show morphological changes characteristic of apoptosis while the number of the cells that undergo cell division and express B-cell lymphoma-2 (Bcl-2) is very low. We suggest that the integrity of nuclear lipid microdomains is important for the response to glucocorticoids of cancer cells.
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