Protocadherin-PC promotes androgen-independent prostate cancer cell growth

Terry, Stéphane; Queires, Luis Carlos Soares; Gil‐Diez‐de‐Medina, Sixtina; Chen, Min-Wei; Taille, Alexandre de la; Allory, Yves; Tran, Phuong-Lan; Abbou, Claude C.; Buttyan, Ralph; Vacherot, Francis

doi:10.1002/pros.20446

Cited by 33 publications

(27 citation statements)

References 42 publications

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“…In a mouse model of colorectal cancer, in which mutated REST was identified as an underlying cause of loss of adhesiveness, no neuronal target genes encoding adhesion molecules were identified (Westbrook et al, 2005). Interestingly, SACO analysis identified a large family of adhesion proteins, protocadherins, which have been associated with human prostate and colon cancers (Okazaki et al, 2002;Yang et al, 2005;Terry et al, 2006). It will be interesting to determine whether they are also dysregulated in the colorectal mouse models.…”

Section: Discussionmentioning

confidence: 99%

A New Binding Motif for the Transcriptional Repressor REST Uncovers Large Gene Networks Devoted to Neuronal Functions

Otto¹,

McCorkle²,

Hover³

et al. 2007

Journal of Neuroscience

213

262

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The repressor element 1 (RE1) silencing transcription factor (REST) helps preserve the identity of nervous tissue by silencing neuronal genes in non-neural tissues. Moreover, in an epithelial model of tumorigenesis, loss of REST function is associated with loss of adhesion, suggesting the aberrant expression of REST-controlled genes encoding this property. To date, no adhesion molecules under REST control have been identified. Here, we used serial analysis of chromatin occupancy to perform genome-wide identification of REST-occupied target sequences (RE1 sites) in a kidney cell line. We discovered novel REST-binding motifs and found that the number of RE1 sites far exceeded previous estimates. A large family of targets encoding adhesion proteins was identified, as were genes encoding signature proteins of neuroendocrine tumors. Unexpectedly, genes considered exclusively non-neuronal also contained an RE1 motif and were expressed in neurons. This supports the model that REST binding is a critical determinant of neuronal phenotype.

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Section: Discussionmentioning

confidence: 99%

A New Binding Motif for the Transcriptional Repressor REST Uncovers Large Gene Networks Devoted to Neuronal Functions

Otto¹,

McCorkle²,

Hover³

et al. 2007

Journal of Neuroscience

213

262

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“…Transcription of PCDH11Y is upregulated in apoptosis-resistant cell variants compared with the parental prostate carcinoma cell line LNCaP. PCDH11Y mRNA levels are increased in androgen-refractory prostate cancers, and its ectopic expression in human prostate cancer cell lines induced anchorageindependent growth in hormone-deprived medium and tumorigenicity in castrated nude mice (Terry et al 2006). Its expression correlated with occurrence of nuclear b-catenin and with increased TCF/Lef transcriptional activity (Yang et al 2005;Terry et al 2006).…”

Section: Protocadherins and Cancermentioning

confidence: 99%

“…PCDH11Y mRNA levels are increased in androgen-refractory prostate cancers, and its ectopic expression in human prostate cancer cell lines induced anchorageindependent growth in hormone-deprived medium and tumorigenicity in castrated nude mice (Terry et al 2006). Its expression correlated with occurrence of nuclear b-catenin and with increased TCF/Lef transcriptional activity (Yang et al 2005;Terry et al 2006). Recently, an interesting link was established between Wnt/b-catenin signaling and androgen independence during prostate cancer progression (Placencio et al 2008;Schweizer et al 2008;Wang et al 2008).…”

Section: Protocadherins and Cancermentioning

confidence: 99%

Involvement of Members of the Cadherin Superfamily in Cancer

Berx¹,

Roy²

2009

Cold Spring Harbor Perspectives in Biology

568

489

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We review the role of cadherins and cadherin-related proteins in human cancer. Cellular and animal models for human cancer are also dealt with whenever appropriate. E-cadherin is the prototype of the large cadherin superfamily and is renowned for its potent malignancy suppressing activity. Different mechanisms for inactivating E-cadherin/CDH1 have been identified in human cancers: inherited and somatic mutations, aberrant protein processing, increased promoter methylation, and induction of transcriptional repressors such as Snail and ZEB family members. The latter induce epithelial mesenchymal transition, which is also associated with induction of "mesenchymal" cadherins, a hallmark of tumor progression. VE-cadherin/CDH5 plays a role in tumor-associated angiogenesis. The atypical T-cadherin/ CDH13 is often silenced in cancer cells but up-regulated in tumor vasculature. The review also covers the status of protocadherins and several other cadherin-related molecules in human cancer. Perspectives for emerging cadherin-related anticancer therapies are given.

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“…Interestingly, expression of PCDH-PC increases in patients with HRPC and has been suggested to be a relevant factor to promote androgen independence of tumor cells [52] . Moreover, a previous examination demonstrated the importance of this gene for the acquisition of apoptosis resistance [53] .…”

Section: Protocadherin-pcmentioning

confidence: 99%

Neuroendocrine Differentiation in Prostate Cancer: From Lab to Bedside

et al. 2007

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Objectives: To discuss the current knowledge on induction, production, sustenance and promotion of neuroendocrine differentiation in human prostate cancer. Methods: Review of the literature using PubMed search and scientific journal publications. Results: Morphological evidence explains some functional relationship between neuroendocrine and neoplastic surrounding cells. Transdifferentiation phenomenon and new biochemical pathways could be included in the development of androgen independence and prostate cancer progression. Conclusion: Multiple evidence seems to confirm that a synergistic functional network between epithelial PSA secretory cells and neuroendocrine intraprostatic system is the main trigger for the induction and sustenance of neuroendocrine differentiation. The development of new antineoplastic molecules should consider the multiple interference of the intercellular network.

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Protocadherin-PC promotes androgen-independent prostate cancer cell growth

Abstract: Our findings suggest a novel mechanism for the progression of CaP involving expression of PCDH-PC. This novel protocadherin induces Wnt signaling, promotes malignant behavior and hormone-resistance of CaP cells.

Cited by 33 publications

References 42 publications

A New Binding Motif for the Transcriptional Repressor REST Uncovers Large Gene Networks Devoted to Neuronal Functions

A New Binding Motif for the Transcriptional Repressor REST Uncovers Large Gene Networks Devoted to Neuronal Functions

Involvement of Members of the Cadherin Superfamily in Cancer

Neuroendocrine Differentiation in Prostate Cancer: From Lab to Bedside

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