scholarly journals Fibroblast growth factor and ornithine decarboxylase 5′UTRs enable preferential expression in human prostate cancer cells and in prostate tumors of PTEN−/− transgenic mice

2011 ◽  
Vol 19 (1) ◽  
pp. 19-29 ◽  
Author(s):  
M Moussavi ◽  
N Moshgabadi ◽  
L Fazli ◽  
E Leblanc ◽  
K Zhang ◽  
...  
Keyword(s):  
Prostate Cancer ◽  
Growth Factor ◽  
Transgenic Mice ◽  
Cancer Cells ◽  
Fibroblast Growth Factor ◽  
Ornithine Decarboxylase ◽  
Fibroblast Growth ◽  
Human Prostate Cancer ◽  
Prostate Cancer Cells ◽  
Preferential Expression

scholarly journals SOCS-3 antagonises the proliferative and migratory effects of fibroblast growth factor-2 in prostate cancer by inhibition of p44/p42 MAPK signalling

2010 ◽  
Vol 17 (2) ◽  
pp. 525-538 ◽  
Author(s):  
Martin Puhr ◽  
Frédéric R Santer ◽  
Hannes Neuwirt ◽  
Gemma Marcias ◽  
Alfred Hobisch ◽  
...  
Keyword(s):  
Prostate Cancer ◽  
Growth Factor ◽  
Cancer Cells ◽  
Fibroblast Growth Factor ◽  
Cellular Proliferation ◽  
Mapk Pathway ◽  
Fibroblast Growth Factor 2 ◽  
Fibroblast Growth ◽  
Prostate Cancer Cells ◽  
Stat3 Phosphorylation

Fibroblast growth factor-2 (FGF-2) is highly expressed in prostate cancer. It promotes tumour progression through multiple pathways including those of signal transducers and activators of transcription factor 3 (STAT3), mitogen-activated protein kinases (MAPKs) and Akt. In previous studies, we have reported that STAT3 phosphorylation inversely correlates with suppressor of cytokine signalling-3 (SOCS-3) expression in prostate cancer cells. Recently, it has become evident that SOCS-3-negative regulation is not only limited to the interleukin-6 (IL-6) receptor. We hypothesised that SOCS-3 interferes with FGF signalling, thus influencing the outcome of its action in prostate cancer cells. For this purpose, we treated DU-145 and LNCaP-IL-6+ cells with increasing concentrations of FGF-2, and verified protein phosphorylation. In the presence of FGF-2, neither STAT3, STAT1, nor Akt could be phosphorylated. Solely the p44/p42 MAPK pathway was activated after FGF-2 stimulation. We show for the first time that SOCS-3 interferes with the FGF-2 signalling pathway by modulating p44 and p42 phosphorylation in prostate cancer cells. Decreased SOCS-3 protein expression results in increased MAPK phosphorylation, whereas SOCS-3 overexpression leads to a decreased cellular proliferation and migration. On the basis of the present results, we propose that SOCS-3 is a novel modulator of FGF-2-regulated cellular events in prostate cancer.

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