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Hormonal regulation...
Hormonal regulation of beta(2)-adrenergic receptor level in prostate cancer
- Article/chapterEnglish2008
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LIBRIS-ID:oai:lup.lub.lu.se:212149a5-7977-4914-a83c-b39844c9b9a4
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https://lup.lub.lu.se/record/1187319URI
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https://doi.org/10.1002/pros.20778DOI
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Language:English
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Summary in:English
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Subject category:art swepub-publicationtype
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Subject category:ref swepub-contenttype
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BACKGROUND. Androgen deprivation is the only effective systemic therapy available for patients with prostatic carcinoma, but is associated with a gradual transition to a hormone-refractory prostate cancer (HRCAP) in which ligand-independent activation of the androgen receptor has been implicated. The beta(2)-adrenergic receptor (beta(2)-AR) is a well-known activator of the androgen receptor. METHODS. Prostatic cell lines were analyzed using cDNA micro-array, real time RT-PCR, radioligand binding assay, cAMP measurements, transfection and thymidine incorporation assay. Clinical specimens were studied by immunohistochemistry and Affymetrix microarrays. RESULTS. Here, we show that beta(2)-AR was transiently down-regulated both at mRNA- and protein levels when hormone-sensitive prostate cancer cells, LNCaP, were cultured in steroid stripped medium (charcoal-stripped fetal calf serum) or when the cells were treated with the anti-androgen, bicalutamide (Casodex). The number of beta-adrenergic receptors was modestly up-regulated in androgen independent cell lines (LNCaP-C4, LNCaP-C4-2 and DU145) compared to LNCaP. Triiodothyronine (T3) increased the level of beta(2)-AR and the effect of T3 was inhibited by bicalutamide. Immunohistochemical staining of human prostate specimens showed high expression of beta(2)-AR in glandular, epithelial cells and increased expression in malignant cells compared to benign hyperplasia and normal tissue. Interestingly, beta(2)-AR mRNA was strongly down-regulated by androgen ablation therapy of prostate cancer patients. CONCLUSION. The level of beta(2)-AR was increased by T3 in prostatic adenocarcinoma cells and reduced in prostate cancer patients who had received androgen ablation therapy for 3 months.
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Eide, Turid
(author)
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Krobert, Kurt Allen
(author)
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Levy, Finn Olav
(author)
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Dizeyi, NishtmanLund University,Lunds universitet,Urologi, Malmö (Abrahamsson),Forskargrupper vid Lunds universitet,Urological research, Malmö,Lund University Research Groups(Swepub:lu)kir-dni
(author)
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Bjartell, AndersLund University,Lunds universitet,Urologisk cancerforskning, Malmö,Forskargrupper vid Lunds universitet,Urological cancer, Malmö,Lund University Research Groups(Swepub:lu)kir-abj
(author)
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Abrahamsson, Per-AndersLund University,Lunds universitet,Urologi, Malmö (Abrahamsson),Forskargrupper vid Lunds universitet,Urological research, Malmö,Lund University Research Groups(Swepub:lu)uro-paa
(author)
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Tasken, Kristin Austlid
(author)
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Urologi, Malmö (Abrahamsson)Forskargrupper vid Lunds universitet
(creator_code:org_t)
Related titles
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In:The Prostate: Wiley68:10, s. 1133-11420270-41371097-0045
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