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rdf:type |
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lifeskim:mentions |
umls-concept:C0017262,
umls-concept:C0037083,
umls-concept:C0105770,
umls-concept:C0185117,
umls-concept:C1280500,
umls-concept:C1420644,
umls-concept:C1512505,
umls-concept:C1516170,
umls-concept:C1565860,
umls-concept:C1705000,
umls-concept:C1705323,
umls-concept:C1710082,
umls-concept:C2911684
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pubmed:issue |
10
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pubmed:dateCreated |
2009-10-5
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pubmed:abstractText |
There is current evidence implicating the Wnt/beta-catenin/TCF pathway in breast cancer. We investigated the effect of para- and meta-positional isomers of nitric oxide-releasing aspirin (NO-ASA), and aspirin (ASA) on MCF-7 human breast cancer cell growth and beta-catenin/TCF signaling. The p- and m-NO-ASA isomers strongly inhibited cell growth and beta-catenin/TCF transcriptional activity compared to ASA; the IC50s for growth inhibition were 57+/-4, 193+/-10 and >5000microM, and for transcriptional inhibition they were 12+/-1.8, 75+/-6.5 and >5000microM for p-, m-NO-ASA and ASA, respectively. p-NO-ASA reduced the expression of Wnt/beta-catenin downstream target gene cyclin D1, and total cellular beta-catenin levels. COX-2 expression was induced by p-NO-ASA, protein kinase C inhibitors reversed this induction. p-NO-ASA blocked the cell cycle transition at S to G2/M phase. These studies suggest a targeted chemopreventive/chemotherapeutic potential for NO-ASA against breast cancer.
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pubmed:grant |
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pubmed:language |
eng
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pubmed:journal |
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pubmed:citationSubset |
IM
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pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/Anticarcinogenic Agents,
http://linkedlifedata.com/resource/pubmed/chemical/Aspirin,
http://linkedlifedata.com/resource/pubmed/chemical/Basic Helix-Loop-Helix Leucine...,
http://linkedlifedata.com/resource/pubmed/chemical/CTNNB1 protein, human,
http://linkedlifedata.com/resource/pubmed/chemical/Cyclin D1,
http://linkedlifedata.com/resource/pubmed/chemical/Cyclooxygenase 2,
http://linkedlifedata.com/resource/pubmed/chemical/DNA-Binding Proteins,
http://linkedlifedata.com/resource/pubmed/chemical/TCF4 protein, human,
http://linkedlifedata.com/resource/pubmed/chemical/Transcription Factors,
http://linkedlifedata.com/resource/pubmed/chemical/Wnt Proteins,
http://linkedlifedata.com/resource/pubmed/chemical/beta Catenin,
http://linkedlifedata.com/resource/pubmed/chemical/nitroaspirin
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pubmed:status |
MEDLINE
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pubmed:month |
Nov
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pubmed:issn |
1873-2968
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pubmed:author |
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pubmed:issnType |
Electronic
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pubmed:day |
15
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pubmed:volume |
78
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
1298-304
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pubmed:dateRevised |
2010-11-18
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pubmed:meshHeading |
pubmed-meshheading:19576865-Anticarcinogenic Agents,
pubmed-meshheading:19576865-Aspirin,
pubmed-meshheading:19576865-Basic Helix-Loop-Helix Leucine Zipper Transcription Factors,
pubmed-meshheading:19576865-Breast Neoplasms,
pubmed-meshheading:19576865-Cell Cycle,
pubmed-meshheading:19576865-Cell Line, Tumor,
pubmed-meshheading:19576865-Cell Proliferation,
pubmed-meshheading:19576865-Cyclin D1,
pubmed-meshheading:19576865-Cyclooxygenase 2,
pubmed-meshheading:19576865-DNA-Binding Proteins,
pubmed-meshheading:19576865-Down-Regulation,
pubmed-meshheading:19576865-Enzyme Induction,
pubmed-meshheading:19576865-Female,
pubmed-meshheading:19576865-Genes, Reporter,
pubmed-meshheading:19576865-Humans,
pubmed-meshheading:19576865-Inhibitory Concentration 50,
pubmed-meshheading:19576865-Isomerism,
pubmed-meshheading:19576865-Signal Transduction,
pubmed-meshheading:19576865-Transcription, Genetic,
pubmed-meshheading:19576865-Transcription Factors,
pubmed-meshheading:19576865-Wnt Proteins,
pubmed-meshheading:19576865-beta Catenin
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pubmed:year |
2009
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pubmed:articleTitle |
Nitro-aspirin inhibits MCF-7 breast cancer cell growth: effects on COX-2 expression and Wnt/beta-catenin/TCF-4 signaling.
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pubmed:affiliation |
Department of Physiology and Pharmacology, City University of New York Medical School, 138th Street and Convent Avenue, New York, NY 10031, United States. nnath@nyit.edu
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pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't,
Research Support, N.I.H., Extramural
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