Linked Life Data

10569799

Source:http://linkedlifedata.com/resource/pubmed/id/10569799

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
4
pubmed:dateCreated
1999-12-28
pubmed:abstractText
The trace element nutrient selenium (Se) has been shown to possess cancer-preventive activity in both animal models and humans, but the mechanisms by which this occurs remain to be elucidated. Because angiogenesis is obligatory for the genesis and growth of solid cancers, we investigated, in the study presented here, the hypothesis that Se may exert its cancer-preventive activity, at least in part, by inhibiting cancer-associated angiogenesis. The effects of chemopreventive levels of Se on the intra-tumoral microvessel density and the expression of vascular endothelial growth factor in 1-methyl-1-nitrosourea-induced rat mammary carcinomas and on the proliferation and survival and matrix metalloproteinase activity of human umbilical vein endothelial cells in vitro were examined. Increased Se intake as Se-enriched garlic, sodium selenite, or Se-methylselenocysteine led to a significant reduction of intra-tumoral microvessel density in mammary carcinomas, irrespective of the manner by which Se was provided: continuous exposure (7-wk feeding) with a chemoprevention protocol or acute bolus exposure (3 d) after carcinomas had established. Compared with the untreated controls, significantly lower levels of vascular endothelial growth factor expression were observed in a sizeable proportion of the Se-treated carcinomas. In contrast to the mammary carcinomas, the microvessel density of the uninvolved mammary glands was not altered by Se treatment. In cell culture, direct exposure of human umbilical vein endothelial cells to Se induced cell death predominantly through apoptosis, decreased the gelatinolytic activities of matrix metalloproteinase-2, or both. These results indicate a potential for Se metabolites to inhibit key attributes (proliferation, survival, and matrix degradation) of endothelial cells critical for angiogenic sprouting. Therefore, inhibition of angiogenesis associated with cancer may be a novel mechanism for the anticancer activity of Se in vivo, and multiple mechanisms are probably involved in mediating the anti-angiogenic activity.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Dec
pubmed:issn
0899-1987
pubmed:author
pubmed:copyrightInfo
Copyright 1999 Wiley-Liss, Inc.
pubmed:issnType
Print
pubmed:volume
26
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
213-25
pubmed:dateRevised
2007-11-14
pubmed:meshHeading
pubmed-meshheading:10569799-Animals, pubmed-meshheading:10569799-Anticarcinogenic Agents, pubmed-meshheading:10569799-Diet, pubmed-meshheading:10569799-Endothelial Growth Factors, pubmed-meshheading:10569799-Endothelium, Vascular, pubmed-meshheading:10569799-Female, pubmed-meshheading:10569799-Garlic, pubmed-meshheading:10569799-Gene Expression Regulation, Neoplastic, pubmed-meshheading:10569799-Humans, pubmed-meshheading:10569799-Lymphokines, pubmed-meshheading:10569799-Mammary Neoplasms, Experimental, pubmed-meshheading:10569799-Methylnitrosourea, pubmed-meshheading:10569799-Microcirculation, pubmed-meshheading:10569799-Neovascularization, Pathologic, pubmed-meshheading:10569799-Neovascularization, Physiologic, pubmed-meshheading:10569799-Phytotherapy, pubmed-meshheading:10569799-Plants, Medicinal, pubmed-meshheading:10569799-Rats, pubmed-meshheading:10569799-Rats, Sprague-Dawley, pubmed-meshheading:10569799-Selenium, pubmed-meshheading:10569799-Sodium Selenite, pubmed-meshheading:10569799-Stromal Cells, pubmed-meshheading:10569799-Umbilical Veins, pubmed-meshheading:10569799-Vascular Endothelial Growth Factor A, pubmed-meshheading:10569799-Vascular Endothelial Growth Factors
pubmed:year
1999
pubmed:articleTitle
Selenium-induced inhibition of angiogenesis in mammary cancer at chemopreventive levels of intake.
pubmed:affiliation
Center for Cancer Causation and Prevention, AMC Cancer Research Center, Denver, Colorado 80214, USA.
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S., Research Support, U.S. Gov't, Non-P.H.S., Research Support, Non-U.S. Gov't