scholarly journals TRP-Channels and Human Prostate Carcinogenesis

Author(s):  
Vyacheslav Lehenkyi ◽  
Natalia Prevarskay
2010 ◽  
Vol 10 ◽  
pp. 1597-1611 ◽  
Author(s):  
Carl Van Haute ◽  
Dirk De Ridder ◽  
Bernd Nilius

This review gives an overview of morphological and functional characteristics in the human prostate. It will focus on the current knowledge about transient receptor potential (TRP) channels expressed in the human prostate, and their putative role in normal physiology and prostate carcinogenesis. Controversial data regarding the expression pattern and the potential impact of TRP channels in prostate function, and their involvement in prostate cancer and other prostate diseases, will be discussed.


2002 ◽  
Vol 1 (1) ◽  
pp. 30
Author(s):  
Peter Mulders ◽  
Geert van Leenders ◽  
Bianca Ory ◽  
Tilly Aalders ◽  
Frans Debruyne ◽  
...  

2016 ◽  
Vol 64 (4) ◽  
pp. 928.1-928 ◽  
Author(s):  
D Hu ◽  
W Hu ◽  
S Majumdar ◽  
T Gauntner ◽  
Y Li ◽  
...  

Estrogens are implicated in prostate development and cancer, while stem cells are essential in tissue homeostasis and carcinogenesis. We have previously demonstrated that estradiol-17β (E2) treatment augments prostaspheres (PS) number and size, implicating them as direct estrogen targets. The present studies sought to elucidate specific roles for ERα and ERβ in prostate stem and progenitor cells.Prostate stem-progenitor cells were identified and isolated from normal primary prostate epithelial cells (PrEC) using long term BrdU retention in 3-D PS culture. FACS analyses (BrdU/ERα or ERβ) showed prostate stem and progenitor populations were both ERα+ and ERβ+. BrdU-retaining stem cells expressed high levels of ERβ and lower ERα as compared to non-label-retaining progenitor cells, suggesting ERβ dominance in the prostate stem cell. Estradiol increased BrdU-retaining cell numbers by enhancing stem cell self-renewal through symmetric division. While ERα siRNA blocked the E2-stimulated BrdU-retaining cells, ERβ knockdown augmented the E2-induced increase of BrdU-retaining cells. Together these findings suggest that ERα stimulates whereas ERβ suppresses stem cell self-renew. This conclusion is supported by separate studies on 2-D cultured PrEC with FACS stem-like cell side-population analysis using selective ER antagonists and siRNA. Although ERβ siRNA did not influence ERα mRNA levels, ERα siRNA doubled ERβ expression suggesting a suppressive role of ERα on ERβ action.In total, the present findings identify distinct localization patterns and roles for ERα and ERβ in human prostate stem-like and daughter progenitor cells with ERα driving self-renewal and ERβ braking division. We propose that a delicate balance between ERα and ERβ contributes to prostate stem cell niche homeostasis and that their dysregulation may contribute to prostate carcinogenesis and progression.


2006 ◽  
Vol 963 (1) ◽  
pp. 156-168 ◽  
Author(s):  
GIUSEPPE CARRUBA ◽  
ROSALBA STEFANO ◽  
LETIZIA COCCIADIFERRO ◽  
FRANCESCA SALADINO ◽  
ANTONIETTA CRISTINA ◽  
...  

Oncogene ◽  
2019 ◽  
Vol 39 (8) ◽  
pp. 1797-1806 ◽  
Author(s):  
Carolyn J. Loveridge ◽  
Sarah Slater ◽  
Kirsteen J. Campbell ◽  
Noor A. Nam ◽  
John Knight ◽  
...  

AbstractBRF1 is a rate-limiting factor for RNA Polymerase III-mediated transcription and is elevated in numerous cancers. Here, we report that elevated levels of BRF1 associate with poor prognosis in human prostate cancer. In vitro studies in human prostate cancer cell lines demonstrated that transient overexpression of BRF1 increased cell proliferation whereas the transient downregulation of BRF1 reduced proliferation and mediated cell cycle arrest. Consistent with our clinical observations, BRF1 overexpression in a Pten-deficient mouse (PtenΔ/ΔBRF1Tg) prostate cancer model accelerated prostate carcinogenesis and shortened survival. In PtenΔ/ΔBRF1Tg tumours, immune and inflammatory processes were altered, with reduced tumoral infiltration of neutrophils and CD4 positive T cells, which can be explained by decreased levels of complement factor D (CFD) and C7 components of the complement cascade, an innate immune pathway that influences the adaptive immune response. We tested if the secretome was involved in BRF1-driven tumorigenesis. Unbiased proteomic analysis on BRF1-overexpresing PC3 cells confirmed reduced levels of CFD in the secretome, implicating the complement system in prostate carcinogenesis. We further identify that expression of C7 significantly correlates with expression of CD4 and has the potential to alter clinical outcome in human prostate cancer, where low levels of C7 associate with poorer prognosis.


2018 ◽  
Author(s):  
Venkatesh Kolluru ◽  
Ashish Tyagi ◽  
Balaji Chandrasekaran ◽  
Murali K. Ankem ◽  
Chendil Damodaran

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