Linked Life Data

11467831

Source:http://linkedlifedata.com/resource/pubmed/id/11467831

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
4
pubmed:dateCreated
2001-7-24
pubmed:abstractText
An increasing amount of evidence suggests that elevated PCho levels are related to the transforming properties of the H-Ras oncoprotein. Based on these observations, we have designed an antitumor strategy using choline kinase, the enzyme responsible of PCho production, as a novel target for drug discovery. However, little relationship between this lipid-related pathway and the other two Ras members, N- and K-ras, has been established. Since N- and K-ras are the most frequently mutated ras genes in human tumors, we have analyzed the PC-PLD/ChoK pathway and the sensitivity to ChoK inhibition of all three ras-transformed cells. Here we demonstrate that transformation by the three Ras oncoproteins results in increased levels of PCho to a similar extent, resulting from a similar constitutive increase of ChoK activity. As well, sensitivity to choline kinase inhibitors as antiproliferative drugs is similar in cell lines transformed by each of the three ras oncogenes, being in all cases higher than parental, nontransformed cells. In addition, H, K and N-ras-induced alterations in PC metabolism is discussed. These results indicate that ChoK can be used as a general target for anticancer drug design against Ras-dependent tumorigenesis.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Jul
pubmed:issn
0006-291X
pubmed:author
pubmed:copyrightInfo
Copyright 2001 Academic Press.
pubmed:issnType
Print
pubmed:day
27
pubmed:volume
285
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
873-9
pubmed:dateRevised
2006-11-15
pubmed:meshHeading
pubmed:year
2001
pubmed:articleTitle
Inhibition of ChoK is an efficient antitumor strategy for Harvey-, Kirsten-, and N-ras-transformed cells.
pubmed:affiliation
Instituto de Investigaciones Biomédicas, CSIC, Madrid, Spain.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't