Linked Life Data

9615775

Source:http://linkedlifedata.com/resource/pubmed/id/9615775

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
2A
pubmed:dateCreated
1998-6-18
pubmed:abstractText
In this study, we investigate the effect of bioflavonoids on the activity and phosphotyrosine content of oncogenic proline-directed protein kinase FA (PDPK FA) in human prostate carcinoma cells. Chronic treatment of human prostate carcinoma cells with low concentrations of quercetin, apigenin, and kaempferol commonly and potently induced tyrosine dephosphorylation and concurrent inactivated oncogenic PDPK FA in a concentration-dependent manner. This is demonstrated by a specific assay of this kinase's activity in the immunoprecipitates from the cell extracts followed by immunoblotting and phosphotyrosine analysis. The results indicate that bioflavonoids may function as common tyrosine kinase inhibitors to inhibit PDPK FA-specific tyrosine kinase and thereby to induce tyrosine dephosphorylation/inactivation of this oncogenic kinase in human carcinoma cells. Under this condition, quercetin, apigenin, and kaempferol can also inhibit cell growth in a similar concentration-dependent manner. The results further indicate that inhibition of tyrosine phosphorylation/activation of this oncogenic PDPK represents a new mode of action mechanism for bioflavonoids during the antiproliferation process in human carcinoma cells.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:issn
0250-7005
pubmed:author
pubmed:issnType
Print
pubmed:volume
18
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
1117-21
pubmed:dateRevised
2009-11-19
pubmed:meshHeading
pubmed:articleTitle
Bioflavonoids commonly and potently induce tyrosine dephosphorylation/inactivation of oncogenic proline-directed protein kinase FA in human prostate carcinoma cells.
pubmed:affiliation
Department of Life Science, National Tsing Hua University, Hsinchu, Taiwan, R.O.C.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't