Document Detail

Does melatonin induce apoptosis in MCF-7 human breast cancer cells in vitro?
MedLine Citation:
PMID:  12071473     Owner:  NLM     Status:  MEDLINE    
Melatonin inhibits proliferation of the estrogen-responsive MCF-7 human breast cancer cells. The objective of this work was to assess whether melatonin not only regulates MCF-7 cell proliferation but also induces apoptosis. In this experiment we used 1,25-dihydroxycholecalciferol (D3) as a positive control because it inhibits MCF-7 cell proliferation and induces apoptosis. MCF-7 cells were cultured with either I nM melatonin, 100 nM D3 or its diluent to determine their effects on cell proliferation, cell viability, cell-cycle phase distribution, population of apoptotic cells, and expression of p53, p21WAF1, bcl-2, bcl-X(L) and bax proteins. After 24 or 48 hr of incubation, both melatonin and D3-treatment significantly decreased the number of viable cells in relation to the controls, although no differences in cell viability were observed between the treatments. The incidence of apoptosis, measured as the population of cells falling in the sub-G1 region of the DNA histogram, or by the TUNEL reaction, was similar in melatonin-treated and control cells whereas, as expected, apoptosis was higher among cells treated with D3 than in controls. The expression of p53 and p21WAF1 proteins significantly increased after 24 or 48 hr of incubation with either melatonin or D3. No significant changes in bcl-2, bcl-XL and bax mRNAs were detected after treatment with melatonin whereas in D3-treated cells, a significant drop in bcl-XL was observed. These data support the hypothesis that melatonin reduces MCF-7 cell proliferation by modulating cell-cycle length through the control of the p53-p21 pathway, but without clearly inducing apoptosis.
Samuel Cos; Maria Dolores Mediavilla; Rosario Fernández; Domingo González-Lamuño; Emilio J Sánchez-Barceló
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't    
Journal Detail:
Title:  Journal of pineal research     Volume:  32     ISSN:  0742-3098     ISO Abbreviation:  J. Pineal Res.     Publication Date:  2002 Mar 
Date Detail:
Created Date:  2002-06-19     Completed Date:  2002-11-08     Revised Date:  2006-11-15    
Medline Journal Info:
Nlm Unique ID:  8504412     Medline TA:  J Pineal Res     Country:  Denmark    
Other Details:
Languages:  eng     Pagination:  90-6     Citation Subset:  IM    
Department of Physiology, School of Medicine, University of Cantabria, Santander, Spain.
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MeSH Terms
Apoptosis / drug effects*
Breast Neoplasms / drug therapy,  metabolism,  pathology*
Cell Cycle / drug effects
Cell Division / drug effects
Cholecalciferol / pharmacology
Cyclin-Dependent Kinase Inhibitor p21
Cyclins / drug effects,  metabolism
Gene Expression Regulation, Neoplastic / drug effects
Melatonin / pharmacology*
Proto-Oncogene Proteins / drug effects,  genetics
Proto-Oncogene Proteins c-bcl-2 / drug effects,  genetics
Tumor Cells, Cultured
Tumor Suppressor Protein p53 / drug effects,  metabolism
bcl-2-Associated X Protein
bcl-X Protein
Reg. No./Substance:
0/BAX protein, human; 0/BCL2L1 protein, human; 0/CDKN1A protein, human; 0/Cyclin-Dependent Kinase Inhibitor p21; 0/Cyclins; 0/Proto-Oncogene Proteins; 0/Proto-Oncogene Proteins c-bcl-2; 0/Tumor Suppressor Protein p53; 0/bcl-2-Associated X Protein; 0/bcl-X Protein; 67-97-0/Cholecalciferol; 73-31-4/Melatonin

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

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