Source:http://linkedlifedata.com/resource/pubmed/id/17364555
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rdf:type | |
lifeskim:mentions | |
pubmed:issue |
1
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pubmed:dateCreated |
2007-3-16
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pubmed:abstractText |
Although androgen-hypersensitivity is one of the possible pathways of hormone-resistance in prostate cancer, the mechanisms of androgen-hypersensitivity are still largely unknown. Using androgen-hypersensitive prostate cancer cells LN-TR2, established from androgen-sensitive LNCaP cells by the long term treatment with tumor necrosis factor alpha, we explored the mechanisms of androgen-hypersensitivity in prostate cancer cells which may thus play a role in hormone-resistance. We examined the androgen receptor (AR) DNA sequence and the expression levels of AR and 8 AR cofactors in LNCaP and LN-TR2 cells. As a result, no novel mutation was developed in AR DNA in LN-TR2 cells. We observed higher expressions of nuclear AR upon androgen-treatment and 2 AR coactivators, ARA55 and TIF2, in LN-TR2 compared to LNCaP cells. An overexpression of ARA55 or TIF2 enhanced androgen-induced AR transcriptional activity in LNCaP cell. In the presence of those AR coactivators, AR activity was observed even at low concentrations of androgen. In 2 of 6 patients, the expression level of ARA55 was higher in cancer cells in hormone-resistant tumor than those in hormone-sensitive tumor. Taken together, our results suggest that prostate cancer cells change androgen-sensitivity by an overexpression of nuclear AR and AR coactivators, thus, resulting in transition from androgen-dependent to androgen-independent prostate cancer cells. An increase in nuclear AR and AR coactivators may cause androgen-hypersensitivity of prostate cancer cells and thus play a role in hormone-resistance, at least in some patients with prostate cancer.
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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/Antineoplastic Agents, Hormonal,
http://linkedlifedata.com/resource/pubmed/chemical/Intracellular Signaling Peptides...,
http://linkedlifedata.com/resource/pubmed/chemical/LIM Domain Proteins,
http://linkedlifedata.com/resource/pubmed/chemical/NCOA2 protein, human,
http://linkedlifedata.com/resource/pubmed/chemical/Nuclear Receptor Coactivator 2,
http://linkedlifedata.com/resource/pubmed/chemical/Receptors, Androgen,
http://linkedlifedata.com/resource/pubmed/chemical/TGFB1I1 protein, human,
http://linkedlifedata.com/resource/pubmed/chemical/Tumor Necrosis Factor-alpha
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pubmed:status |
MEDLINE
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pubmed:month |
Feb
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pubmed:issn |
0735-7907
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pubmed:author | |
pubmed:issnType |
Print
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pubmed:volume |
25
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
32-7
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pubmed:dateRevised |
2011-11-17
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pubmed:meshHeading |
pubmed-meshheading:17364555-Androgen Antagonists,
pubmed-meshheading:17364555-Antineoplastic Agents, Hormonal,
pubmed-meshheading:17364555-Blotting, Western,
pubmed-meshheading:17364555-Cell Line, Tumor,
pubmed-meshheading:17364555-Cell Nucleus,
pubmed-meshheading:17364555-Drug Resistance, Neoplasm,
pubmed-meshheading:17364555-Humans,
pubmed-meshheading:17364555-Immunohistochemistry,
pubmed-meshheading:17364555-Intracellular Signaling Peptides and Proteins,
pubmed-meshheading:17364555-LIM Domain Proteins,
pubmed-meshheading:17364555-Male,
pubmed-meshheading:17364555-Neoplasms, Hormone-Dependent,
pubmed-meshheading:17364555-Nuclear Receptor Coactivator 2,
pubmed-meshheading:17364555-Prostatic Neoplasms,
pubmed-meshheading:17364555-Receptors, Androgen,
pubmed-meshheading:17364555-Reverse Transcriptase Polymerase Chain Reaction,
pubmed-meshheading:17364555-Transfection,
pubmed-meshheading:17364555-Tumor Necrosis Factor-alpha
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pubmed:year |
2007
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pubmed:articleTitle |
Prostate cancer cells increase androgen sensitivity by increase in nuclear androgen receptor and androgen receptor coactivators; a possible mechanism of hormone-resistance of prostate cancer cells.
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pubmed:affiliation |
Department of Urology, School of Medicine, University of Occupational and Environmental Health, Kitakyushu, Japan. n.fuji@med.uoeh-u.ac.jp
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pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't
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