Prostate‐derived factor as a paracrine and autocrine factor for the proliferation of androgen receptor‐positive human prostate cancer cells

. Its downstream p52Shc , ERK1/2, Akt, Src, STAT-3, and STAT-5 were activated, and cell proliferation, proliferating cell nuclear antigen, and cyclin D1 expression were increased. Stable subclones of C-33 cells by small interfering PAcP had elevated Tyr 1221/2 phosphorylation of ErbB-2 and exhibited androgen-independent growth and increased tumorigenicity in xenograft female animals. In summary, our data together indicate that in prostate epithelia, cPAcP interacts with and dephosphorylates ErbB-2 primarily at Tyr 1221/2 and hence blocks downstream signaling, leading to reduced cell growth. In PCa cells, decreased cPAcP expression is associated with androgen-independent cell proliferation and tumorigenicity as seen in advanced hormone-refractory prostate carcinomas.

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“…Y, tyrosine. tained in BRFF-HPC1 medium supplemented with 20% FBS, 2 mM glutamine, and 50 g/ml gentamicin (37).…”

Section: Methodsmentioning

confidence: 99%

Human Prostatic Acid Phosphatase, an Authentic Tyrosine Phosphatase, Dephosphorylates ErbB-2 and Regulates Prostate Cancer Cell Growth

Chuang

Chen

Lin

et al. 2010

Journal of Biological Chemistry

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110

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“…Prostate-derived factor (PDF), is a member of the TGF superfamily and also acts as a paracrine and autocrine factor to induce proliferation of prostate cancer cells (Chen et al, 2007). Secretion of PDF was shown to induce proliferation and clonogenic growth of androgen receptor positive cells via the ERK1/2 signalling pathway (Chen et al, 2007).…”

Section: 2a Transforming Growth Factor  (Tgf)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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“…MDA PCa2b cells were maintained as described previously (Chen et al, 2007). For AG879 treatment, LNCaP C-81 cells were incubated for 48 h in a steroid-reduced (SR) medium followed by AG879 treatment in an SR condition for another 16 h. Transient transfection were performed using Lipofectamine and plus reagents for LNCaP cells as described previously (Meng et al, 2000).…”

Section: Cell Culture and Transfectionmentioning

confidence: 99%

“…In androgen-independent human PCa cells, ErbB-2 is greatly activated by tyrosyl phosphorylation, at least in part due to the low or null expression of cellular prostatic acid phosphatase (cPAcP), a prostate-unique tyrosine phosphatase that dephosphorylates ErbB-2 . Increased ErbB-2 activity in PCa cells correlated with their androgen-independent proliferation, anchorage-independent growth and tumorigenicity (Igawa et al, 2002;Veeramani et al, 2005;Chen et al, 2007). ErbB-2 may also promote the adhesion of prostate cells (Vafa et al, 1998) while the underlying molecular basis is not understood.…”

Section: Introductionmentioning

confidence: 99%

ErbB-2 via PYK2 upregulates the adhesive ability of androgen receptor-positive human prostate cancer cells

et al. 2007

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Aberrant regulation in the adhesive ability of cancer cells is closely associated with their metastatic activity. In this study, we examine the role of ErbB-2 in regulating the adhesive ability of androgen receptor (AR)-positive human prostate cancer (PCa) cells, the major cell population of PCa. Utilizing different LNCaP and MDA PCa2b cells as model systems, we found that ErbB-2 activity was correlated with PYK2 activity and adhesive ability in those cells. Increased ErbB-2 expression or activity in LNCaP C-33 cells enhanced PYK2 activation and cell adhesion, while the high PYK2 activity and the rapid adhesion of LNCaP C-81 cells were decreased by diminishing ErbB-2 expression or activity. Knockdown studies revealed the predominant role of ErbB-2 in regulating LNCaP C-81 cell adhesion. Coimmunoprecipitation showed that C-81 cells had increased interaction between ErbB-2 and PYK2. Elevated ErbB-2 activity in LNCaP cells correlated with increased ERK/MAPK activity and enhanced adhesive ability, which were abolished by the expression of K457A-PYK2 mutant or the treatment of PD98059, a MEK inhibitor. In summary, our data suggested that ErbB-2, via PYK2-ERK/MAPK, upregulates the adhesive ability of AR-positive human PCa cells.

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Prostate‐derived factor as a paracrine and autocrine factor for the proliferation of androgen receptor‐positive human prostate cancer cells

Abstract: PDF promotes AR-positive prostate tumor progression through upregulating cell proliferation via ERK1/2 signal pathway.

Cited by 66 publications

References 43 publications

Human Prostatic Acid Phosphatase, an Authentic Tyrosine Phosphatase, Dephosphorylates ErbB-2 and Regulates Prostate Cancer Cell Growth

Human Prostatic Acid Phosphatase, an Authentic Tyrosine Phosphatase, Dephosphorylates ErbB-2 and Regulates Prostate Cancer Cell Growth

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

ErbB-2 via PYK2 upregulates the adhesive ability of androgen receptor-positive human prostate cancer cells

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