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rdf:type |
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lifeskim:mentions |
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pubmed:issue |
1
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pubmed:dateCreated |
2009-9-28
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pubmed:abstractText |
We examined the efficacy of combination treatments utilizing cytotoxic drugs plus inhibitors to members of the ErbB-ERK signal pathway in human prostate cancer (PCa) LNCaP C-81 cells. Under an androgen-reduced condition, 50nM gemcitabine caused about 40% growth suppression on C-81 cells. Simultaneous treatment of gemcitabine plus 10microM AG825 produced 60% suppression (p<0.03); while, 85% growth inhibition (p<0.02) was seen if AG825 was added to gemcitabine-treated cells after a 24h-interval. Our data thus showed that in androgen-reduced conditions, inhibition of ErbB-2 increases the cytotoxic efficacy of gemcitabine in PCa cells. This finding has significant implications in the choice of drugs for combination therapy as well as the order of administration for treating cancer patients.
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pubmed:grant |
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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 |
http://linkedlifedata.com/resource/pubmed/chemical/Androgens,
http://linkedlifedata.com/resource/pubmed/chemical/Antimetabolites, Antineoplastic,
http://linkedlifedata.com/resource/pubmed/chemical/BAX protein, human,
http://linkedlifedata.com/resource/pubmed/chemical/BCL2L1 protein, human,
http://linkedlifedata.com/resource/pubmed/chemical/Benzothiazoles,
http://linkedlifedata.com/resource/pubmed/chemical/Deoxycytidine,
http://linkedlifedata.com/resource/pubmed/chemical/ERBB2 protein, human,
http://linkedlifedata.com/resource/pubmed/chemical/Extracellular Signal-Regulated MAP...,
http://linkedlifedata.com/resource/pubmed/chemical/Flavonoids,
http://linkedlifedata.com/resource/pubmed/chemical/PD 98059,
http://linkedlifedata.com/resource/pubmed/chemical/Protein Kinase Inhibitors,
http://linkedlifedata.com/resource/pubmed/chemical/Proto-Oncogene Proteins c-bcl-2,
http://linkedlifedata.com/resource/pubmed/chemical/Receptor, erbB-2,
http://linkedlifedata.com/resource/pubmed/chemical/Tyrphostins,
http://linkedlifedata.com/resource/pubmed/chemical/bcl-2-Associated X Protein,
http://linkedlifedata.com/resource/pubmed/chemical/bcl-X Protein,
http://linkedlifedata.com/resource/pubmed/chemical/gemcitabine,
http://linkedlifedata.com/resource/pubmed/chemical/tyrphostin AG 1478,
http://linkedlifedata.com/resource/pubmed/chemical/tyrphostin AG825
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pubmed:status |
MEDLINE
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pubmed:month |
Nov
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pubmed:issn |
1872-7980
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pubmed:author |
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pubmed:issnType |
Electronic
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pubmed:day |
18
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pubmed:volume |
285
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
58-65
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pubmed:dateRevised |
2011-9-26
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pubmed:meshHeading |
pubmed-meshheading:19467571-Androgens,
pubmed-meshheading:19467571-Antimetabolites, Antineoplastic,
pubmed-meshheading:19467571-Antineoplastic Combined Chemotherapy Protocols,
pubmed-meshheading:19467571-Apoptosis,
pubmed-meshheading:19467571-Benzothiazoles,
pubmed-meshheading:19467571-Cell Line, Tumor,
pubmed-meshheading:19467571-Cell Proliferation,
pubmed-meshheading:19467571-Deoxycytidine,
pubmed-meshheading:19467571-Dose-Response Relationship, Drug,
pubmed-meshheading:19467571-Down-Regulation,
pubmed-meshheading:19467571-Extracellular Signal-Regulated MAP Kinases,
pubmed-meshheading:19467571-Flavonoids,
pubmed-meshheading:19467571-Humans,
pubmed-meshheading:19467571-Male,
pubmed-meshheading:19467571-Prostatic Neoplasms,
pubmed-meshheading:19467571-Protein Kinase Inhibitors,
pubmed-meshheading:19467571-Proto-Oncogene Proteins c-bcl-2,
pubmed-meshheading:19467571-Receptor, erbB-2,
pubmed-meshheading:19467571-Time Factors,
pubmed-meshheading:19467571-Tyrphostins,
pubmed-meshheading:19467571-bcl-2-Associated X Protein,
pubmed-meshheading:19467571-bcl-X Protein
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pubmed:year |
2009
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pubmed:articleTitle |
Suppression of ErbB-2 in androgen-independent human prostate cancer cells enhances cytotoxic effect by gemcitabine in an androgen-reduced environment.
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pubmed:affiliation |
Department of Biochemistry and Molecular Biology, University of Nebraska Medical Center, Omaha, 68198-5870, USA.
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pubmed:publicationType |
Journal Article,
Research Support, U.S. Gov't, Non-P.H.S.,
Research Support, N.I.H., Extramural
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