Source:http://linkedlifedata.com/resource/pubmed/id/19885579
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rdf:type | |
lifeskim:mentions | |
pubmed:issue |
6
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pubmed:dateCreated |
2009-11-3
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pubmed:abstractText |
E-selectin is expressed on the surfaces of stimulated vascular endothelial cells and is sometimes involved in cancer cell metastasis. The H2-receptor antagonist cimetidine inhibits the increase in E-selectin expression on vascular endothelial cells that is induced by interleukin-1beta (IL-1beta) and cimetidine. It also inhibits the adhesion of sialyl-Lewis-antigen-positive cancer cells to vascular endothelial cells, ultimately inhibiting hematogenous metastasis. Anticancer drugs are essential to cancer therapy, but whether they can alter the expression of E-selectin in vascular endothelial cells remains unclear. Whether cimetidine inhibits the expression of E-selectin in the same manner in the presence or absence of anticancer drugs also remains unknown. Human umbilical vein endothelial cells were cultured with 5-fluorouracil (5-FU), doxorubicin (DXR), cisplatin (CDDP), or IL-1beta and with or without cimetidine. The expression of E-selectin at the mRNA and protein levels was then determined using quantitative reverse transcription-polymerase chain reaction and immunohistochemical staining, respectively. The E-selectin mRNA level increased in cells exposed to 5-FU, DXR, or CDDP, but the addition of cimetidine had no effect on the E-selectin mRNA level. The expression of E-selectin protein was also significantly higher after the addition of 5-FU, DXR, or CDDP, compared with that of a negative control. However, when cimetidine was added prior to the addition of 5-FU, DXR, or CDDP, the expression of E-selectin was significantly suppressed. Thus, cimetidine significantly inhibited the expression of E-selectin at the protein level without affecting its expression at the mRNA level in cells treated with anticancer drugs. In conclusion, anticancer drugs increased the expression of E-selectin and this increase was inhibited by cimetidine. These findings suggest that the administration of cimetidine during treatment with anticancer drugs might be useful for preventing metastasis.
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pubmed:language |
eng
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pubmed:journal | |
pubmed:citationSubset |
IM
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pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/Actins,
http://linkedlifedata.com/resource/pubmed/chemical/Antineoplastic Agents,
http://linkedlifedata.com/resource/pubmed/chemical/Cimetidine,
http://linkedlifedata.com/resource/pubmed/chemical/Cisplatin,
http://linkedlifedata.com/resource/pubmed/chemical/Doxorubicin,
http://linkedlifedata.com/resource/pubmed/chemical/E-Selectin,
http://linkedlifedata.com/resource/pubmed/chemical/Enzyme Inhibitors,
http://linkedlifedata.com/resource/pubmed/chemical/Fluorouracil
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pubmed:status |
MEDLINE
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pubmed:month |
Dec
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pubmed:issn |
1791-2431
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pubmed:author | |
pubmed:issnType |
Electronic
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pubmed:volume |
22
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
1293-7
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pubmed:meshHeading |
pubmed-meshheading:19885579-Actins,
pubmed-meshheading:19885579-Antineoplastic Agents,
pubmed-meshheading:19885579-Cimetidine,
pubmed-meshheading:19885579-Cisplatin,
pubmed-meshheading:19885579-Dose-Response Relationship, Drug,
pubmed-meshheading:19885579-Doxorubicin,
pubmed-meshheading:19885579-E-Selectin,
pubmed-meshheading:19885579-Endothelial Cells,
pubmed-meshheading:19885579-Enzyme Inhibitors,
pubmed-meshheading:19885579-Fluorouracil,
pubmed-meshheading:19885579-Humans,
pubmed-meshheading:19885579-Immunohistochemistry,
pubmed-meshheading:19885579-Neoplasm Metastasis,
pubmed-meshheading:19885579-Polymerase Chain Reaction,
pubmed-meshheading:19885579-Umbilical Veins
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pubmed:year |
2009
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pubmed:articleTitle |
Increase in E-selectin expression in umbilical vein endothelial cells by anticancer drugs and inhibition by cimetidine.
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pubmed:affiliation |
Department of General and Gastrointestinal Surgery, School of Medicine, Fujita Health University, Aichi, Japan.
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pubmed:publicationType |
Journal Article
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