Document Detail

Magnesium depletion causes growth inhibition, reduced expression of cyclin D1, and increased expression of P27Kip1 in normal but not in transformed mammary epithelial cells.
MedLine Citation:
PMID:  10395294     Owner:  NLM     Status:  MEDLINE    
In this study, we have evaluated the effects of extracellular magnesium restriction on the growth and cell cycle parameters of normal (HC11) and transformed (MCF-7) breast epithelial cell lines. Cells were incubated in medium with different concentrations of Mg2+ (from 0.5 to 0 mM) and the growth rates were determined by [3H]-thymidine incorporation and cell counting. The growth of the HC11 cells was drastically inhibited by Mg2+ depletion whereas the MCF-7 cells were only slightly inhibited (about 50% and 15%, respectively, after incubation in 0.05 mM Mg for 48 h). Cell cycle analyses showed a decrease in the percentage of cells in the S phase when both cell lines were incubated at low Mg2+ concentration. However, while the percentage of cells in both the G0/G1 and G2/M phases was increased in the HC11 cells, only the percentage of cells in the G2/M phase was increased in the MCF-7 cell line. Extracellular magnesium depletion was associated with increased expression of the cyclin-dependent kinase inhibitor p27Kip1 and decreased expression of cyclin D1 in the HC11 but not in the MCF-7 cells. We also demonstrated that Mg2+ depletion does not inhibit kinase activities in the normal HC11 cells and that Mg2+-restricted HC11 cells are still responsive to the epidermal growth factor (EGF)- and insulin-mediated stimulation of cell growth. These data suggest that normal but not transformed mammary epithelial cells are inhibited by extracellular Mg2+ restriction and that this effect might be mediated by changes in the levels of expression of both cyclin D1 and p27Kip1.
A Sgambato; F I Wolf; B Faraglia; A Cittadini
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Publication Detail:
Type:  Comparative Study; Journal Article; Research Support, Non-U.S. Gov't    
Journal Detail:
Title:  Journal of cellular physiology     Volume:  180     ISSN:  0021-9541     ISO Abbreviation:  J. Cell. Physiol.     Publication Date:  1999 Aug 
Date Detail:
Created Date:  1999-07-16     Completed Date:  1999-07-16     Revised Date:  2006-11-15    
Medline Journal Info:
Nlm Unique ID:  0050222     Medline TA:  J Cell Physiol     Country:  UNITED STATES    
Other Details:
Languages:  eng     Pagination:  245-54     Citation Subset:  IM    
Centro di Ricerche Oncologiche Giovanni XXIII, Istituto di Patologia Generale, Università Cattolica del Sacro Cuore, Rome, Italy.
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MeSH Terms
Breast Neoplasms
Cell Cycle Proteins*
Cell Division / drug effects,  physiology
Cell Line, Transformed / cytology,  drug effects,  enzymology
Cyclin D1 / genetics*
Cyclin E / genetics
Cyclin-Dependent Kinase Inhibitor p27
Enzyme Inhibitors / metabolism*
Flow Cytometry
G0 Phase / drug effects
Gene Expression Regulation, Neoplastic / drug effects*
Magnesium / pharmacology*
Mammary Glands, Animal / cytology*
Mice, Inbred BALB C
Microtubule-Associated Proteins / genetics*
S Phase / drug effects
Thymidine / metabolism,  pharmacology
Tritium / diagnostic use
Tumor Suppressor Proteins*
Reg. No./Substance:
0/Cdkn1b protein, mouse; 0/Cell Cycle Proteins; 0/Cyclin E; 0/Enzyme Inhibitors; 0/Microtubule-Associated Proteins; 0/Tumor Suppressor Proteins; 10028-17-8/Tritium; 136601-57-5/Cyclin D1; 147604-94-2/Cyclin-Dependent Kinase Inhibitor p27; 50-89-5/Thymidine; 7439-95-4/Magnesium

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine

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