Linked Life Data

10741730

Source:http://linkedlifedata.com/resource/pubmed/id/10741730

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
3
pubmed:dateCreated
2000-6-1
pubmed:abstractText
Initial clinic studies revealed that proline-directed protein kinase FA (PDPK FA) is overexpressed manyfold in various human cancerous tissues relative to the normal control. However, the role of overexpressed PDPK FA in cancers remains unknown and needs to be established. To determine whether PDPK FA is associated with drug sensitivity, we investigated the effects of partial inhibition of this kinase on the human prostate carcinoma cell line (PC-3). PDPK FA antisense expression vector and its specific antibody were successfully developed. Two stable transfected antisense clones (PA7 and PA3) of human prostate carcinoma cell were subcloned, and they expressed approximately 75% and approximately 35% of the total PDPK FA existing in the control-transfected clone as determined by both immunoprecipitate activity assay and immunoblot analysis. In sharp contrast, the PDPK FA antisense clones expressed no significant suppression of any other related proline-directed protein kinase member expression, demonstrating the specificity of these two antisense clones. When compared with parental or control-transfected cells, the low-PDPK FA-expressing antisense clones displayed an enhanced sensitivity to carboplatin, 5-fluorouracil, paclitaxel, and hydroxyurea. Estimation of the IC50 index further revealed that the antisense clones displayed up to > 100-fold drug sensitivity, and there was a correlation between suppressed levels of PDPK FA and drug sensitivity. Taken together, the results demonstrate that specific antisense suppression of overexpressed PDPK FA in human prostate cancer cells is sufficient to enhance various drug sensitivity, indicating that PDPK FA is an important regulator in controlling multiple drug resistance of human prostate cancer cells.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Mar
pubmed:issn
1078-0432
pubmed:author
pubmed:issnType
Print
pubmed:volume
6
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
1024-30
pubmed:dateRevised
2009-11-19
pubmed:meshHeading
pubmed-meshheading:10741730-Antineoplastic Agents, pubmed-meshheading:10741730-Carboplatin, pubmed-meshheading:10741730-Cell Survival, pubmed-meshheading:10741730-Cisplatin, pubmed-meshheading:10741730-DNA, Antisense, pubmed-meshheading:10741730-DNA, Complementary, pubmed-meshheading:10741730-DNA, Recombinant, pubmed-meshheading:10741730-Dose-Response Relationship, Drug, pubmed-meshheading:10741730-Fluorouracil, pubmed-meshheading:10741730-Gene Expression Regulation, Enzymologic, pubmed-meshheading:10741730-Genetic Vectors, pubmed-meshheading:10741730-Humans, pubmed-meshheading:10741730-Hydroxyurea, pubmed-meshheading:10741730-Male, pubmed-meshheading:10741730-Paclitaxel, pubmed-meshheading:10741730-Proline-Directed Protein Kinases, pubmed-meshheading:10741730-Prostatic Neoplasms, pubmed-meshheading:10741730-Protein-Serine-Threonine Kinases, pubmed-meshheading:10741730-Transfection, pubmed-meshheading:10741730-Tumor Cells, Cultured
pubmed:year
2000
pubmed:articleTitle
Antisense suppression of proline-directed protein kinase FA enhances chemosensitivity in human prostate cancer cells.
pubmed:affiliation
Department of Life Science, National Tsing Hua University, Hsinchu, Taiwan, Republic of China.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't