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Predicate | Object |
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rdf:type | |
lifeskim:mentions | |
pubmed:issue |
6
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pubmed:dateCreated |
1995-7-18
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pubmed:abstractText |
Both androgen and antiandrogen treatments enhance the proliferation rate of the hormone-dependent prostate cancer cell line LNCaP, expressing a mutated androgen receptor (AR). We studied the modification of the expression of epidermal growth factor (EGF), of its receptor (EGF-R), and of androgen receptor (AR) in the LNCaP cell line, under basal conditions and during androgen (R1881) and antiandrogen hydroxy-flutamide (OH-FLU) treatment. After prolonged R1881 administration, a marked increase of EGF release was observed, completely blocked by the addition of OH-FLU. The Scatchard plot analysis of EGF-R binding revealed two classes of binding sites with high and low affinity. The administration of OH-FLU alone or combined with R1881 did not modify the affinity constants, while the low-affinity component disappeared after androgen administration. Both androgen and antiandrogen administration led to a significant increase of the EGF-R high-affinity component. AR mRNA and protein levels were downregulated by R1881 treatment. Following OH-FLU administration, AR mRNA was slightly downregulated, and there was not a strict parallelism between AR mRNA levels and AR binding capacity. When combined with R1881, OH-FLU partially counteracted the androgen-induced AR downregulation. Our data show that EGF-R binding capacity is the only parameter constantly raised in cell proliferation with respect to quiescent cells, and highlights the nonunivocal action of OH-FLU on androgen-induced effects.
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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/Androgen Antagonists,
http://linkedlifedata.com/resource/pubmed/chemical/Epidermal Growth Factor,
http://linkedlifedata.com/resource/pubmed/chemical/Flutamide,
http://linkedlifedata.com/resource/pubmed/chemical/Metribolone,
http://linkedlifedata.com/resource/pubmed/chemical/RNA, Messenger,
http://linkedlifedata.com/resource/pubmed/chemical/Receptor, Epidermal Growth Factor,
http://linkedlifedata.com/resource/pubmed/chemical/Receptors, Androgen,
http://linkedlifedata.com/resource/pubmed/chemical/hydroxyflutamide
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pubmed:status |
MEDLINE
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pubmed:month |
Jun
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pubmed:issn |
0270-4137
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pubmed:author | |
pubmed:issnType |
Print
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pubmed:volume |
26
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pubmed:owner |
NLM
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pubmed:authorsComplete |
N
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pubmed:pagination |
290-8
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pubmed:dateRevised |
2009-11-19
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pubmed:meshHeading |
pubmed-meshheading:7784269-Androgen Antagonists,
pubmed-meshheading:7784269-Blotting, Northern,
pubmed-meshheading:7784269-Down-Regulation,
pubmed-meshheading:7784269-Epidermal Growth Factor,
pubmed-meshheading:7784269-Flutamide,
pubmed-meshheading:7784269-Gene Expression,
pubmed-meshheading:7784269-Humans,
pubmed-meshheading:7784269-Male,
pubmed-meshheading:7784269-Metribolone,
pubmed-meshheading:7784269-Prostatic Neoplasms,
pubmed-meshheading:7784269-Protein Binding,
pubmed-meshheading:7784269-RNA, Messenger,
pubmed-meshheading:7784269-Radioimmunoassay,
pubmed-meshheading:7784269-Receptor, Epidermal Growth Factor,
pubmed-meshheading:7784269-Receptors, Androgen,
pubmed-meshheading:7784269-Time Factors,
pubmed-meshheading:7784269-Tumor Cells, Cultured
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pubmed:year |
1995
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pubmed:articleTitle |
Androgenic and antiandrogenic control on epidermal growth factor, epidermal growth factor receptor, and androgen receptor expression in human prostate cancer cell line LNCaP.
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pubmed:affiliation |
Department of Experimental Medicine, University of L'Aquila, Italy.
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pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't
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