Linked Life Data

17364555

Source:http://linkedlifedata.com/resource/pubmed/id/17364555

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
1
pubmed:dateCreated
2007-3-16
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.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Feb
pubmed:issn
0735-7907
pubmed:author
pubmed:issnType
Print
pubmed:volume
25
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
32-7
pubmed:dateRevised
2011-11-17
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
pubmed:year
2007
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.
pubmed:affiliation
Department of Urology, School of Medicine, University of Occupational and Environmental Health, Kitakyushu, Japan. n.fuji@med.uoeh-u.ac.jp
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't