Distribution of vascular endothelial growth factor (VEGF) in prostate disease

Walsh, Kilian; Sriprasad, Seshadri; Hopster, Deborah J.; Codd, Jonathan R.; Mulvin, D.

doi:10.1038/sj.pcan.4500575

Cited by 28 publications

(24 citation statements)

References 21 publications

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“…This suggests that stromal-endothelial cell interactions in the regulation of angiogenesis are different from one setting to another and depend upon the other factors in the environment. Increasing expression of VEGF in the spectrum of PC growth may reflect an active role for epithelial VEGF in this process, similar to that suggested in BPH [22]. VEGF and FGF are the angiogenic factors that are expressed most frequently in tumors, and have been shown to act synergistically bFGF is actively synthesized in the human prostate [23].…”

Section: Discussionmentioning

confidence: 87%

Microvessel density and regulators of angiogenesis in malignant and nonmalignant prostate tissue

et al. 2006

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The aim of this study was to investigate the relationship between microvessel density (MVD), positive and negative angiogenic factors, and established prognostic factors in prostate cancer (PC), and, to clarify the effect of angiogenic factors to angiogenesis. The vascularization of neoplastic, non-neoplastic prostate tissue was determined by CD34 immunostaining. Angiogenetic mediators VEGF, bFGF, TSP-1, and p53 were studied by immunohistochemistry. Neovascularization and p53, VEGF, and TSP-1 expressions of tumorous tissue were higher than non-tumorous tissue. The bFGF expression in these tissues was not different. The p53 expression was not correlated with the expressions of VEGF, bFGF, and TSP-1 in PC. Our results demonstrate a significant increase in MVD, VEGF, TSP-1, and p53 expressions in prostate tumorigenesis. The pretreatment sPSA was the only parameter demonstrating significant correlation with tumor grade and may have a value in the prediction of aggressive tumor behavior in PC.

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Section: Discussionmentioning

confidence: 87%

Microvessel density and regulators of angiogenesis in malignant and nonmalignant prostate tissue

et al. 2006

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“…VEGF has been implicated in tumor progression and expression of VEGF has been reported in a number of cell lines and clinical specimens derived from a broad range of cancers (30–33). Here we examined whether exposure to SM stimulated VEGF secretion in prostate cancer cells.…”

Section: Resultsmentioning

confidence: 99%

Cigarette smoke induces nuclear translocation of heme oxygenase 1 (HO-1) in prostate cancer cells: Nuclear HO-1 promotes vascular endothelial growth factor secretion

Birrane

Yang

et al. 2013

International Journal of Oncology

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Prostate cancer is the second leading cause of male-cancer related death in the United States. Despite a number of evidence-based studies which strongly suggest an association between cigarette smoking and prostate cancer, the underlying biological mechanism is largely unknown. Heme oxygenase 1 (HO-1) has been implicated in maintaining cellular homeostasis, but also in tumor angiogenesis. Nuclear HO-1 protein expression has been observed in various types of tumors including prostate cancer. These studies, however, were reported as clinical and pathological observations, and failed to investigate nuclear HO-1 at the molecular level in cancer. The present study explores the relationship between cigarette smoke and nuclear HO-1-modulated promotion of vascular endothelial growth factor (VEGF) secretion. We have demonstrated that cigarette smoke medium (SM)-induced HO-1 mRNA expression and upregulated HO-1 protein levels in the prostate cancer cell lines DU145 and PC3. We also observed that SM significantly induced nuclear expression of HO-1, and enhanced secretion of VEGF in cells. Nuclear-directed expression of HO-1 activated the transcriptional activity of VEGF and promoted VEGF secretion in prostate cancer cells. This study provides new insights into the molecular mechanism by which cigarette smoke-induced nuclear translocation of HO-1 promotes VEGF secretion in prostate cancer cells. Nuclear HO-1 may, therefore, constitute an attractive therapeutic target to inhibit angiogenesis and the progression of prostate cancer.

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“…VEGF and TNF-a (Lissbrant et al, 2001;Walsh et al, 2002), on the ET-1 secretion by HPEC. Furthermore, we were interested whether the vasoactive adenosine triphosphate (ATP) has any influence on such an ET-1 secretion.…”

Section: Introductionmentioning

confidence: 97%

The Secretion of Endothelin-1 by Microvascular Endothelial Cells from Human Benign Prostatic Hyperplasia is Inhibited by Vascular Endothelial Growth Factor

et al. 2004

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Prostate growth seems to be influenced by paracrine factors like endothelin-1 (ET-1), originating from the microvascular endothelium. Recently, we reported on the first isolation and primary culture of microvascular endothelial cells (HPEC) derived from tissue of human benign prostatic hyperplasia (BPH). Therefore, direct investigation of growth factor secretion by HPEC is now possible. BPH tissue was cut into small cubes and gently squeezed after incubation with dispase. HPEC were cultured from the resulting cell suspension after a stepwise selection by use of superparamagnetic beads coated with antibodies against endothelial specific antigens. HPEC were characterized by flow cytometry. After the incubation of HPEC either with vascular endothelial growth factor (VEGF), tumor necrosis factor alpha (TNF-alpha), or adenosine triphosphate (ATP), the secretion of ET-1 was measured by ELISA. HPEC showed a typical endothelial morphology. They were positive for von Willebrand factor and CD31. The ET-1 secretion of HPEC was inhibited by VEGF, but was unaffected by TNF-alpha or ATP. Furthermore, histochemistry revealed that in vivo microvascular endothelial cells were negative for ET-1. Because of the suppression by the widespread VEGF, it is unlikely that ET-1 from the microvascular endothelium acts as a growth factor in human BPH.

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Distribution of vascular endothelial growth factor (VEGF) in prostate disease

Cited by 28 publications

References 21 publications

Microvessel density and regulators of angiogenesis in malignant and nonmalignant prostate tissue

Microvessel density and regulators of angiogenesis in malignant and nonmalignant prostate tissue

Cigarette smoke induces nuclear translocation of heme oxygenase 1 (HO-1) in prostate cancer cells: Nuclear HO-1 promotes vascular endothelial growth factor secretion

The Secretion of Endothelin-1 by Microvascular Endothelial Cells from Human Benign Prostatic Hyperplasia is Inhibited by Vascular Endothelial Growth Factor

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