Next Article in Journal
Differential Proteomics Analysis of Bacillus amyloliquefaciens and Its Genome-Shuffled Mutant for Improving Surfactin Production
Next Article in Special Issue
Interactions of Borneol with DPPC Phospholipid Membranes: A Molecular Dynamics Simulation Study
Previous Article in Journal
Evaluating the Role of PTH in Promotion of Chondrosarcoma Cell Proliferation and Invasion by Inhibiting Primary Cilia Expression
Previous Article in Special Issue
FT-IR Microspectrometry Reveals the Variation of Membrane Polarizability due to Epigenomic Effect on Epithelial Ovarian Cancer
Article Menu
Issue 11 (November) cover image

Export Article

Open AccessArticle
Int. J. Mol. Sci. 2014, 15(11), 19832-19846;

Nuclear Lipid Microdomain as Resting Place of Dexamethasone to Impair Cell Proliferation

Laboratory of Nuclear Lipid BioPathology, Crabion, 06074 Perugia, Italy
Department of Pharmaceutical Science, University of Perugia, 06100 Perugia, Italy
Laboratory of Clinical Pathology, 96011 Augusta-Siracusa, Italy
Department of Biology, University of Pisa, 56127 Pisa, Italy
Department of Clinical and Biological Sciences, University of Udine, 33100 Udine, Italy
These authors contributed equally to this work.
Author to whom correspondence should be addressed.
Received: 13 September 2014 / Revised: 24 October 2014 / Accepted: 27 October 2014 / Published: 31 October 2014
(This article belongs to the Special Issue Bioactive Lipids and Lipidomics)
Full-Text   |   PDF [1571 KB, uploaded 31 October 2014]   |  


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. View Full-Text
Keywords: dexametasone; lymphoma; nuclear lipid microdomains; sphingomyelin; sphingomyelinase; sphingomyelin-synthase dexametasone; lymphoma; nuclear lipid microdomains; sphingomyelin; sphingomyelinase; sphingomyelin-synthase

Figure 1

This is an open access article distributed under the Creative Commons Attribution License which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited (CC BY 4.0).

Share & Cite This Article

MDPI and ACS Style

Cataldi, S.; Codini, M.; Cascianelli, G.; Tringali, S.; Tringali, A.R.; Lazzarini, A.; Floridi, A.; Bartoccini, E.; Garcia-Gil, M.; Lazzarini, R.; Ambesi-Impiombato, F.S.; Curcio, F.; Beccari, T.; Albi, E. Nuclear Lipid Microdomain as Resting Place of Dexamethasone to Impair Cell Proliferation. Int. J. Mol. Sci. 2014, 15, 19832-19846.

Show more citation formats Show less citations formats

Related Articles

Article Metrics

Article Access Statistics



[Return to top]
Int. J. Mol. Sci. EISSN 1422-0067 Published by MDPI AG, Basel, Switzerland RSS E-Mail Table of Contents Alert
Back to Top