Expression profiling of androgen-dependent and -independent LNCaP cells: EGF versus androgen signalling

Oosterhoff, Josien K; Grootegoed, J. Anton; Blok, Leen J.

doi:10.1677/erc.1.00897

Cited by 24 publications

(16 citation statements)

References 40 publications

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“…Even then, depletion of ERG in VCaP cells resulted in only a small increase (<25%) in the androgen-induced expression of genes such as FKBP51, SLC45A3 and TMPRSS2 (Yu et al, 2010). Increased expression of androgen-regulated genes has been previously reported in androgen-independent prostate cancer cells (Gregory et al, 1998;Oosterhoff et al, 2005;Dehm and Tindall, 2006).…”

Section: Increased Basal Expression Of Several Ar Target Genes In Vcamentioning

confidence: 83%

Androgen receptor amplification is reflected in the transcriptional responses of Vertebral-Cancer of the Prostate cells

Makkonen

Kauhanen

Jääskeläinen

et al. 2011

Molecular and Cellular Endocrinology

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Please cite this article as: Makkonen, H., Kauhanen, M., Jääskeläinen, T., Palvimo, J.J., Androgen receptor amplification is reflected in the transcriptional responses of Vertebral-Cancer of the Prostate cells, Molecular and Cellular Endocrinology (2010), doi:10.1016/j.mce.2010 This is a PDF file of an unedited manuscript that has been accepted for publication. As a service to our customers we are providing this early version of the manuscript. The manuscript will undergo copyediting, typesetting, and review of the resulting proof before it is published in its final form. Please note that during the production process errors may be discovered which could affect the content, and all legal disclaimers that apply to the journal pertain.

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Section: Increased Basal Expression Of Several Ar Target Genes In Vcamentioning

confidence: 83%

Androgen receptor amplification is reflected in the transcriptional responses of Vertebral-Cancer of the Prostate cells

Makkonen

Kauhanen

Jääskeläinen

et al. 2011

Molecular and Cellular Endocrinology

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“…Other regulatory pathways may also be involved. For example, EGF signaling, which downregulates UGT2B17 expression without affecting UGT2B15 in LNCaP cells (23), has been identified as a transduction pathway involved in prostate tumor growth (33,34).…”

Section: Discussionmentioning

confidence: 99%

Androgen Glucuronidation: An Unexpected Target for Androgen Deprivation Therapy, with Prognosis and Diagnostic Implications

et al. 2013

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Androgen deprivation therapy (ADTh) remains a mainstay of prostate cancer treatment, but its efficacy is bypassed by mechanisms that are not fully understood. In human prostate cancer cells, androgen glucuronidation, catalyzed by the two UDP-glucuronosyltransferase (UGT) enzymes UGT2B15 and UGT2B17, is the major androgen inactivation pathway. In this study, we investigated the effect of ADTh on androgen glucuronidation to evaluate its potential clinical utility for prostate cancer prognosis or therapy. UGT2B15 and UGT2B17 expression was evaluated in prostate cancer specimens from untreated or treated patients and in cell models of prostate cancer exposed to clinically relevant antiandrogens. UGT2B15 and UGT2B17 protein levels in prostate were increased after 5 months of ADTh when compared with specimens from untreated patients. UGT2B15 expression remained elevated for up to 12 months, but UGT2B17 returned to initial levels as soon as after 6 months. Several androgen receptor (AR) antagonists tested caused a dose-and time-dependent stimulation of UGT2B15 and UGT2B17 expression and androgen glucuronidation in prostate cancer cell lines. The role of AR in these regulatory events was confirmed using AR-deficient LNCaP cells, in which UGT2B attenuation reduced the antiproliferative effects of AR pharmacologic antagonists. Through this combination of clinical and functional investigations, our work revealed that ADTh stimulates a local androgen metabolism in prostate cells, establishing a foundation to evaluate the potential of UGT2B15 and UGT2B17 as drug targets and/or molecular markers for ADTh responsiveness and maintenance in prostate cancer. Cancer Res; 73(23); 6963-71. Ó2013 AACR.

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“…In the LNCaP cell line, both EGF and androgen could induce cell cycle regulated genes. Of those genes, 75% were the same suggesting EGF can stimulate androgen-regulated genes in the absence of androgen (Oosterhoff et al, 2005).…”

Section: 2d Epidermal Growth Factor (Egf)mentioning

confidence: 99%

Androgen receptor signalling in prostate: Effects of stromal factors on normal and cancer stem cells

Berry

Maitland

Collins

2008

Molecular and Cellular Endocrinology

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Please cite this article as: Berry, P.A., Maitland, N.J., Collins, A.T., Androgen receptor signalling in prostate: effects of stromal factors on normal and cancer stem cells, Molecular and Cellular Endocrinology (2007), doi:10.1016/j.mce.2008 This is a PDF file of an unedited manuscript that has been accepted for publication. As a service to our customers we are providing this early version of the manuscript. The manuscript will undergo copyediting, typesetting, and review of the resulting proof before it is published in its final form. Please note that during the production process errors may be discovered which could affect the content, and all legal disclaimers that apply to the journal pertain. AbstractThe prostate gland is the most common site for cancer in males within the developed world. Androgens play a vital role in prostate development, maintenance of tissue function and pathogenesis of prostate disease. The androgen receptor signalling pathway facilitates that role in both the epithelial compartment and in the underlying stroma. Stroma is a key mediator of androgenic effects upon the epithelium and can regulate both the fate of the epithelial stem cell and potentially the initiation and progression of prostate cancer. Different groups of growth factors are expressed by stroma, which control proliferation, and differentiation of prostate epithelium demonstrating a critical role for stroma in epithelial growth and homeostasis. Paracrine stromal proteins may offer the possibility to control tumour stem cell growth and could permit prostate-specific targeting of both therapies and of androgenresponsive proteins. The effect of 5-dihydrotestosterone, the more potent metabolite of testosterone, on expression of androgen regulated genes in stroma from benign prostatic hyperplasia is a key mediator of epithelial cell fate. Global gene expression arrays have recently identified new candidate genes in androgen responsive stroma, some of which have androgen receptor binding sites in their promoter regions. Some of these genes have direct androgen receptor binding ability.

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Expression profiling of androgen-dependent and -independent LNCaP cells: EGF versus androgen signalling

Cited by 24 publications

References 40 publications

Androgen receptor amplification is reflected in the transcriptional responses of Vertebral-Cancer of the Prostate cells

Androgen receptor amplification is reflected in the transcriptional responses of Vertebral-Cancer of the Prostate cells

Androgen Glucuronidation: An Unexpected Target for Androgen Deprivation Therapy, with Prognosis and Diagnostic Implications

Androgen receptor signalling in prostate: Effects of stromal factors on normal and cancer stem cells

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