Source:http://linkedlifedata.com/resource/pubmed/id/12888923
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rdf:type | |
lifeskim:mentions |
umls-concept:C0017262,
umls-concept:C0021467,
umls-concept:C0021469,
umls-concept:C0034392,
umls-concept:C0040688,
umls-concept:C0086418,
umls-concept:C0185117,
umls-concept:C0205263,
umls-concept:C0242275,
umls-concept:C0334227,
umls-concept:C0376358,
umls-concept:C0596290,
umls-concept:C1292733,
umls-concept:C2677316,
umls-concept:C2911684
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pubmed:issue |
3
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pubmed:dateCreated |
2003-7-30
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pubmed:abstractText |
Because ErbB-2 receptor is involved in hormone-independency for growth and metastasis of prostate cancer cells, the aim was to investigate the effects of quercetin on ErbB-2 and ErbB-3 expression and its critical components such as MAP kinase and PI-3 kinase. Hemocytometric counts and [3H]-thymidine incorporation were used to determine the effects of quercetin, EGF and TGF-alpha on cell proliferation and DNA synthesis in PC-3 and LnCap cells. Changes in ErbB-2, ErbB-3 and components of MAPK and PI-3K pathways were analyzed by Western blot analysis. Treatment of PC-3 and LnCap cells with quercetin resulted in a dose-dependent growth inhibition. The rate of DNA synthesis was decreased by 40, 55 and 65% on treatment with 14.5, 29.0 and 58.0 microM of quercetin, respectively. Concomitantly, these treatments led to a dose-dependent decrease in ErbB-2, ErbB-3 and their basal autophosphorylation levels as compared to controls. Cyclin D1 expression and basal phosphorylation of c-Raf, MAPK, Elk-1 and Akt-1 in PC-3 cells was also inhibited by quercetin treatment. Co-treating PC-3 cells with quercetin significantly attenuated EGF- and TGF-alpha-induced growth and phosphorylation of ErbB-2, ErbB-3, c-Raf, MAPK kinase 1/2 (MEK1/2), MAPK, Elk-1 and Akt-1. Since ErbB receptor is important for growth, metastasis and drug resistance, inhibition of ErbB-2 and ErbB-3 by pharmacological doses of quercetin may provide a new approach for treatment of prostate cancers.
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pubmed:language |
eng
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pubmed:journal | |
pubmed:citationSubset |
IM
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pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/Cyclin D1,
http://linkedlifedata.com/resource/pubmed/chemical/DNA,
http://linkedlifedata.com/resource/pubmed/chemical/Epidermal Growth Factor,
http://linkedlifedata.com/resource/pubmed/chemical/Phosphatidylinositol 3-Kinases,
http://linkedlifedata.com/resource/pubmed/chemical/Proto-Oncogene Proteins c-raf,
http://linkedlifedata.com/resource/pubmed/chemical/Quercetin,
http://linkedlifedata.com/resource/pubmed/chemical/Receptor, erbB-2,
http://linkedlifedata.com/resource/pubmed/chemical/Receptor, erbB-3,
http://linkedlifedata.com/resource/pubmed/chemical/Transforming Growth Factor alpha
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pubmed:status |
MEDLINE
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pubmed:month |
Sep
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pubmed:issn |
1019-6439
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pubmed:author | |
pubmed:issnType |
Print
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pubmed:volume |
23
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
821-9
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pubmed:dateRevised |
2010-11-18
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pubmed:meshHeading |
pubmed-meshheading:12888923-Blotting, Western,
pubmed-meshheading:12888923-Cell Division,
pubmed-meshheading:12888923-Cell Line, Tumor,
pubmed-meshheading:12888923-Cyclin D1,
pubmed-meshheading:12888923-DNA,
pubmed-meshheading:12888923-Dose-Response Relationship, Drug,
pubmed-meshheading:12888923-Epidermal Growth Factor,
pubmed-meshheading:12888923-Humans,
pubmed-meshheading:12888923-MAP Kinase Signaling System,
pubmed-meshheading:12888923-Male,
pubmed-meshheading:12888923-Phosphatidylinositol 3-Kinases,
pubmed-meshheading:12888923-Phosphorylation,
pubmed-meshheading:12888923-Prostatic Neoplasms,
pubmed-meshheading:12888923-Proto-Oncogene Proteins c-raf,
pubmed-meshheading:12888923-Quercetin,
pubmed-meshheading:12888923-Receptor, erbB-2,
pubmed-meshheading:12888923-Receptor, erbB-3,
pubmed-meshheading:12888923-Transforming Growth Factor alpha
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pubmed:year |
2003
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pubmed:articleTitle |
Inhibition of ErbB-2 and ErbB-3 expression by quercetin prevents transforming growth factor alpha (TGF-alpha)- and epidermal growth factor (EGF)-induced human PC-3 prostate cancer cell proliferation.
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pubmed:affiliation |
Laboratory of Molecular Endocrinology, Division of Cellular and Molecular Research, National Cancer Centre of Singapore, Singapore 169610, Republic of Singapore. cmrhth@nccs.com.sg
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pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't
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