scholarly journals TMPRSS2, a Serine Protease Expressed in the Prostate on the Apical Surface of Luminal Epithelial Cells and Released into Semen in Prostasomes, Is Misregulated in Prostate Cancer Cells

2010 ◽  
Vol 176 (6) ◽  
pp. 2986-2996 ◽  
Author(s):  
Ya-Wen Chen ◽  
Ming-Shyue Lee ◽  
Amanda Lucht ◽  
Feng-Pai Chou ◽  
Wei Huang ◽  
...  
Keyword(s):  
Prostate Cancer ◽  
Epithelial Cells ◽  
Cancer Cells ◽  
Serine Protease ◽  
Apical Surface ◽  
Prostate Cancer Cells ◽  
Luminal Epithelial Cells

scholarly journals Regenerated Luminal Epithelial Cells Are Derived from Preexisting Luminal Epithelial Cells in Adult Mouse Prostate

2011 ◽  
Vol 25 (11) ◽  
pp. 1849-1857 ◽  
Author(s):  
June Liu ◽  
Laura E. Pascal ◽  
Sudhir Isharwal ◽  
Daniel Metzger ◽  
Raquel Ramos Garcia ◽  
...  
Keyword(s):  
Prostate Cancer ◽  
Epithelial Cells ◽  
Cancer Cells ◽  
Androgen Deprivation Therapy ◽  
Specific Antigen ◽  
Androgen Deprivation ◽  
Genetic Lineage ◽  
Prostate Cancer Cells ◽  
Mouse Prostate ◽  
Luminal Epithelial Cells

Abstract Determining the source of regenerated luminal epithelial cells in the adult prostate during androgen deprivation and replacement will provide insights into the origin of prostate cancer cells and their fate during androgen deprivation therapy. Prostate stem cells in the epithelial layer have been suggested to give rise to luminal epithelium. However, the extent of stem cell participation to prostate regrowth is not clear. In this report, using prostate-specific antigen-CreERT2-based genetic lineage marking/tracing in mice, preexisting luminal epithelial cells were shown to be a source of regenerated luminal epithelial cells in the adult prostate. Prostatic luminal epithelial cells could survive androgen deprivation and were capable of proliferating upon androgen replacement. Prostate cancer cells, typically exhibiting a luminal epithelial phenotype, may retain this intrinsic capability to survive and regenerate in response to changes in androgen signaling, providing part of the mechanism for the ultimate failure of androgen deprivation therapy in prostate cancer.

Basal prostate epithelial cells stimulate the migration of prostate cancer cells

2004 ◽  
Vol 41 (2) ◽  
pp. 85-97 ◽  
Author(s):  
Hsiao-Man Yu ◽  
Diane E. Frank ◽  
Jie Zhang ◽  
Xueke You ◽  
William G. Carter ◽  
...  
Keyword(s):  
Prostate Cancer ◽  
Epithelial Cells ◽  
Cancer Cells ◽  
Prostate Cancer Cells ◽  
Prostate Epithelial Cells

scholarly journals The cytotoxic and pro-apoptotic activities of the novel fluoropyrimidine F10 towards prostate cancer cells are enhanced by Zn2+ -chelation and inhibiting the serine protease Omi/HtrA2

The Prostate ◽  
2014 ◽  
Vol 75 (4) ◽  
pp. 360-369 ◽  
Author(s):  
William H. Gmeiner ◽  
Olcay Boyacioglu ◽  
Christopher H. Stuart ◽  
Jamie Jennings-Gee ◽  
K.C. Balaji
Keyword(s):  
Prostate Cancer ◽  
Cancer Cells ◽  
Serine Protease ◽  
The Novel ◽  
Prostate Cancer Cells

scholarly journals The membrane-anchored serine protease, TMPRSS2, activates PAR-2 in prostate cancer cells

2005 ◽  
Vol 388 (3) ◽  
pp. 967-972 ◽  
Author(s):  
Susan WILSON ◽  
Brett GREER ◽  
John HOOPER ◽  
Andries ZIJLSTRA ◽  
Brian WALKER ◽  
...  
Keyword(s):  
Prostate Cancer ◽  
Cancer Cells ◽  
Serine Protease ◽  
G Protein ◽  
Calcium Mobilization ◽  
Prostate Cancer Cells ◽  
Protease Domain ◽  
Serine Protease Domain ◽  
Pre Treatment ◽  
G Protein Coupled

TMPRSS2 is a type II transmembrane-bound serine protease that has gained interest owing to its highly localized expression in the prostate and its overexpression in neoplastic prostate epithelium. Once activated, the serine protease domain of TMPRSS2 is released from the cell surface into the extracellular space. PAR (protease-activated receptor)-2 belongs to a family of G-protein-coupled receptors (PAR-1–4) that are activated by specific serine proteases, which are expressed in many normal and malignant cell types. Previous in vitro studies on prostate cancer cells suggest a role for PAR-2 in prostate cancer metastasis. A polyclonal anti-human TMPRSS2 antibody was generated against the TMPRSS2 serine protease domain. The antibody showed specific reactivity with recombinant expressed TMPRSS2, and so was used to extract and purify the cleaved active TMPRSS2 protease from prostate cancer cells. Reverse transcriptase PCR and Western blot analysis were used to show the expression of both TMPRSS2 and PAR-2 in the androgen-dependent LNCaP prostate cancer cell line. Treatment of LNCaP cells with the cellular immunopurified TMPRSS2 protease induced a transient increase in intracellular calcium, which is indicative of G-protein-coupled-receptor activation. This calcium mobilization was inhibited by cellular pre-treatment with a specific PAR-2 antagonist, but not with a PAR-1 antagonist; inhibition of the protease activity also failed to mobilize calcium, suggesting that TMPRSS2 is capable of cleaving and thereby activating the PAR-2 receptor. The calcium mobilization was also inhibited by cellular pre-treatment with suramin or 2-APB (2-aminoethoxydiphenyl borate), indicating that a G-protein pathway is involved and that subsequent calcium release is mainly from intracellular stores. The present study describes how TMPRSS2 may contribute to prostate tumour metastasis via the activation of PAR-2.

Effect of androgen signaling in stromal cells on growth of prostate cancer.

2016 ◽  
Vol 34 (2_suppl) ◽  
pp. 297-297 ◽  
Author(s):  
Chun-Peng Liao ◽  
Leng-Ying Chen ◽  
Andrea Luethy ◽  
Youngsoo Kim ◽  
A. Robert MacLeod ◽  
...  
Keyword(s):  
Prostate Cancer ◽  
Epithelial Cells ◽  
Cancer Cells ◽  
Stromal Cells ◽  
Culture System ◽  
Human Prostate ◽  
Human Prostate Cancer ◽  
Prostate Cancer Cells ◽  
Epithelial Cancer ◽  
Mesenchymal Transition

297 Background: Interactions between epithelial and stroma cells are important in the development of prostate cancer (PCa). Cancer-associated fibroblasts (CAFs) have been to support tumor progression, metastasis, and differentiation. Androgen receptor (AR) and related pathways are known to support the growth and survival of prostate epithelial cancer cells, the roles of AR-dependent processes in cancerous stroma are less clear. We sought to investigate if AR-dependent pathways present in CAF cells influence the growth and tumorogencity of epithelial cancer cells in relation to androgen-deprivation therapy in prostate cancer. Methods: Murine CAFs were isolated from a well-described PTEN-dependent cancer mouse model (Liao, et al Cancer Res, 2010. 70(18):7294). A co-culture system was developed based on multiple lines of murine CAFs grown along with human prostate cancer epithelial cells, and a murine-specific anti-sense oligonucleotide (ASO) against murine AR was used to specifically suppress AR expression in murine CAFs in this system. RT-PCR was used to investigate changes in gene expression. Results: Using this co-culture system, we found that murine CAFs promoted cell proliferation and colony formation in several human prostate cancer cell lines. Further, these processes were decreased by suppression of AR-expression in CAFs. Expression of genes related to tumorigenicity in epithelial cells were investigated. Markers associated with epithelial-mesenchymal transition (EMT, N-Cad) and “stemness” (OCT4, Sox2, Nanog) were increased in human prostate cancer cells grown with low-AR CAFs. Conclusions: Our data indicates that suppression of AR in CAFs results in down-regulation in the growth and tumorigenicity of prostate cancer cells through pathways related to EMT and “cell reprograming”. As such, development of therapies which inhibit the tumor-promoting pathways present in stromal cells may be one approach to improve the treatment of prostate cancer.

scholarly journals Gene expression relationship between prostate cancer cells of Gleason 3, 4 and normal epithelial cells as revealed by cell type-specific transcriptomes

BMC Cancer ◽  
2009 ◽  
Vol 9 (1) ◽  
Author(s):  
Laura E Pascal ◽  
Ricardo ZN Vêncio ◽  
Laura S Page ◽  
Emily S Liebeskind ◽  
Christina P Shadle ◽  
...  
Keyword(s):  
Gene Expression ◽  
Prostate Cancer ◽  
Epithelial Cells ◽  
Cancer Cells ◽  
Cell Type ◽  
Prostate Cancer Cells ◽  
Cell Type Specific
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