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rdf:type |
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lifeskim:mentions |
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pubmed:dateCreated |
2010-1-11
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pubmed:abstractText |
Past studies have shown that sensitivity of melanoma cells to TRAIL-induced apoptosis is largely correlated with the expression levels of TRAIL death receptors on the cell surface. However, fresh melanoma isolates and melanoma tissue sections express generally low levels of death receptors for TRAIL. The clinical potential of TRAIL in the treatment of melanoma may therefore be limited unless given with agents that increase the cell surface expression of TRAIL death receptors. 2-Deoxy-D-glucose (2-DG) is a synthetic glucose analogue that inhibits glycolysis and glycosylation and blocks cell growth. It has been in clinical evaluation for its potential use as an anticancer agent. In this study, we have examined whether 2-DG and TRAIL interact to enhance their cytotoxicity towards melanoma cells.
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pubmed:commentsCorrections |
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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 |
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pubmed:status |
MEDLINE
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pubmed:issn |
1476-4598
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pubmed:author |
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pubmed:issnType |
Electronic
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pubmed:volume |
8
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
122
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pubmed:dateRevised |
2010-9-28
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pubmed:meshHeading |
pubmed-meshheading:20003459-Apoptosis,
pubmed-meshheading:20003459-Cell Line, Tumor,
pubmed-meshheading:20003459-DNA-Binding Proteins,
pubmed-meshheading:20003459-Deoxyglucose,
pubmed-meshheading:20003459-Glycosylation,
pubmed-meshheading:20003459-Humans,
pubmed-meshheading:20003459-Melanoma,
pubmed-meshheading:20003459-Receptors, TNF-Related Apoptosis-Inducing Ligand,
pubmed-meshheading:20003459-TNF-Related Apoptosis-Inducing Ligand,
pubmed-meshheading:20003459-Transcription Factors,
pubmed-meshheading:20003459-Up-Regulation
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pubmed:year |
2009
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pubmed:articleTitle |
2-Deoxy-D-glucose enhances TRAIL-induced apoptosis in human melanoma cells through XBP-1-mediated up-regulation of TRAIL-R2.
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pubmed:affiliation |
Immunology and Oncology Unit, Calvary Mater Newcastle Hospital, NSW, Australia. liuhao6886@yahoo.com.cn
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pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't
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