Source:http://linkedlifedata.com/resource/pubmed/id/21596021
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rdf:type | |
lifeskim:mentions |
umls-concept:C0017262,
umls-concept:C0017337,
umls-concept:C0023688,
umls-concept:C0038769,
umls-concept:C0185117,
umls-concept:C0220781,
umls-concept:C0282651,
umls-concept:C0334227,
umls-concept:C0376358,
umls-concept:C0812246,
umls-concept:C1314939,
umls-concept:C1456820,
umls-concept:C1510470,
umls-concept:C1883254,
umls-concept:C1948023,
umls-concept:C2349975,
umls-concept:C2911684
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pubmed:issue |
3
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pubmed:dateCreated |
2011-6-13
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pubmed:abstractText |
Sialyl Lewis x (sLe(x)) plays an important role in cancer metastasis. But, the mechanism for its production in metastatic cancers remains unclear. The objective of current study was to examine the effects of a proinflammatory cytokine on the expression of glycosyltransferase and sulfotransferase genes involved in the synthesis of selectin ligands in a prostate cancer cell line. Androgen-independent human lymph node-derived metastatic prostate cancer cells (C-81 LNCaP), which express functional androgen receptor and mimic the castration-resistant advanced prostate cancer, were used. TNF? treatment of these cells increased their binding to P-, E- and L-selectins, anti-sLe(x) antibody, and anti-6-sulfo-sialyl Lewis x antibody by 12%, 240%, 43%, 248% and 21%, respectively. Also, the expression of C2GnT-1, B4GalT1, GlcNAc6ST3, and ST3Gal3 genes was significantly upregulated. Further treatment of TNF?-treated cells with either anti-sLe(x) antibody or E-selectin significantly suppressed their in vitro migration (81% and 52%, respectively) and invasion (45% and 56%, respectively). Our data indicate that TNF? treatment enhances the motility and invasion properties of LNCaP C-81 cells by increasing the formation of selectin ligands through stimulation of the expression of selective glycosyl- and sulfotransferase genes. These results support the hypothesis that inflammation contributes to cancer metastasis.
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pubmed:grant | |
pubmed:language |
eng
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pubmed:journal | |
pubmed:citationSubset |
IM
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pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/5-acetylneuraminyl-(2-3)-galactosyl-...,
http://linkedlifedata.com/resource/pubmed/chemical/E-Selectin,
http://linkedlifedata.com/resource/pubmed/chemical/Glycosyltransferases,
http://linkedlifedata.com/resource/pubmed/chemical/L-Selectin,
http://linkedlifedata.com/resource/pubmed/chemical/Ligands,
http://linkedlifedata.com/resource/pubmed/chemical/Oligosaccharides,
http://linkedlifedata.com/resource/pubmed/chemical/P-Selectin,
http://linkedlifedata.com/resource/pubmed/chemical/Sulfotransferases,
http://linkedlifedata.com/resource/pubmed/chemical/Tumor Necrosis Factor-alpha
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pubmed:status |
MEDLINE
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pubmed:month |
Jun
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pubmed:issn |
1090-2104
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pubmed:author | |
pubmed:copyrightInfo |
Copyright © 2011 Elsevier Inc. All rights reserved.
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pubmed:issnType |
Electronic
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pubmed:day |
10
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pubmed:volume |
409
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
436-41
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pubmed:meshHeading |
pubmed-meshheading:21596021-Cell Line, Tumor,
pubmed-meshheading:21596021-Cell Movement,
pubmed-meshheading:21596021-E-Selectin,
pubmed-meshheading:21596021-Gene Expression Regulation, Enzymologic,
pubmed-meshheading:21596021-Gene Expression Regulation, Neoplastic,
pubmed-meshheading:21596021-Glycosyltransferases,
pubmed-meshheading:21596021-Humans,
pubmed-meshheading:21596021-L-Selectin,
pubmed-meshheading:21596021-Ligands,
pubmed-meshheading:21596021-Male,
pubmed-meshheading:21596021-Neoplasm Invasiveness,
pubmed-meshheading:21596021-Oligosaccharides,
pubmed-meshheading:21596021-P-Selectin,
pubmed-meshheading:21596021-Prostatic Neoplasms,
pubmed-meshheading:21596021-Sulfotransferases,
pubmed-meshheading:21596021-Tumor Necrosis Factor-alpha
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pubmed:year |
2011
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pubmed:articleTitle |
TNF? enhances the motility and invasiveness of prostatic cancer cells by stimulating the expression of selective glycosyl- and sulfotransferase genes involved in the synthesis of selectin ligands.
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pubmed:affiliation |
Department of Biochemistry and Molecular Biology, College of Medicine, University of Nebraska Medical Center, Omaha, NE 68198, USA.
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pubmed:publicationType |
Journal Article,
Research Support, U.S. Gov't, Non-P.H.S.,
Research Support, Non-U.S. Gov't,
Research Support, N.I.H., Extramural
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