scholarly journals RNAi-mediated gene silencing of vascular endothelial growth factor C suppresses growth and induces apoptosis in mouse breast cancer in vitro and in vivo

2016 ◽  
Vol 12 (5) ◽  
pp. 3896-3904 ◽  
Author(s):  
Yong-Chao Liu ◽  
Wen-Hui Ma ◽  
Yin-Lin Ge ◽  
Mei-Lan Xue ◽  
Zheng Zhang ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Vascular Endothelial Growth Factor ◽  
Growth Factor ◽  
Gene Silencing ◽  
Vascular Endothelial ◽  
Mouse Breast Cancer ◽  
Factor C ◽  
Endothelial Growth Factor

scholarly journals Netrin-4 induces lymphangiogenesis in vivo

Blood ◽  
2010 ◽  
Vol 115 (26) ◽  
pp. 5418-5426 ◽  
Author(s):  
Frederic Larrieu-Lahargue ◽  
Alana L. Welm ◽  
Kirk R. Thomas ◽  
Dean Y. Li
Keyword(s):  
Vascular Endothelial Growth Factor ◽  
Endothelial Cells ◽  
Growth Factor ◽  
Vascular Endothelial ◽  
Lymphatic Endothelial Cells ◽  
Tumor Dissemination ◽  
Factor C ◽  
Endothelial Growth Factor

Abstract Netrin-4, a laminin-related secreted protein is an axon guidance cue recently shown essential outside of the nervous system, regulating mammary and lung morphogenesis as well as blood vascular development. Here, we show that Netrin-4, at physiologic doses, induces proliferation, migration, adhesion, tube formation and survival of human lymphatic endothelial cells in vitro comparable to well-characterized lymphangiogenic factors fibroblast growth factor-2 (FGF-2), hepatocyte growth factor (HGF), vascular endothelial growth factor-A (VEGF-A), and vascular endothelial growth factor-C (VEGF-C). Netrin-4 stimulates phosphorylation of intracellular signaling components Akt, Erk and S6, and their specific inhibition antagonizes Netrin-4–induced proliferation. Although Netrin receptors Unc5B and neogenin, are expressed by human lymphatic endothelial cells, suppression of either or both does not suppress Netrin-4–promoted in vitro effects. In vivo, Netrin-4 induces growth of lymphatic and blood vessels in the skin of transgenic mice and in breast tumors. Its overexpression in human and mouse mammary carcinoma cancer cells leads to enhanced metastasis. Finally, Netrin-4 stimulates in vitro and in vivo lymphatic permeability by activating small GTPases and Src family kinases/FAK, and down-regulating tight junction proteins. Together, these data provide evidence that Netrin-4 is a lymphangiogenic factor contributing to tumor dissemination and represents a potential target to inhibit metastasis formation.

Vascular endothelial growth factor C acts as a neurotrophic factor for dopamine neurons in vitro and in vivo

Neuroscience ◽  
2011 ◽  
Vol 192 ◽  
pp. 550-563 ◽  
Author(s):  
M. Piltonen ◽  
A. Planken ◽  
O. Leskelä ◽  
T.T. Myöhänen ◽  
A.-L. Hänninen ◽  
...  
Keyword(s):  
Vascular Endothelial Growth Factor ◽  
Growth Factor ◽  
Neurotrophic Factor ◽  
Dopamine Neurons ◽  
Vascular Endothelial ◽  
Factor C ◽  
Endothelial Growth Factor

Regulation of Vascular Endothelial Growth Factor by Tamoxifen in vitro and in vivo

2003 ◽  
Vol 55 (2) ◽  
pp. 119-124 ◽  
Author(s):  
Michael D. Mueller ◽  
Elizabeth A. Pritts ◽  
Charles J. Zaloudek ◽  
Ekkehard Dreher ◽  
Robert N. Taylor
Keyword(s):  
Vascular Endothelial Growth Factor ◽  
Growth Factor ◽  
Vascular Endothelial ◽  
Endothelial Growth Factor

Vascular Endothelial Growth Factor Inhibits the Development of Dendritic Cells and Dramatically Affects the Differentiation of Multiple Hematopoietic Lineages In Vivo

Blood ◽  
1998 ◽  
Vol 92 (11) ◽  
pp. 4150-4166 ◽  
Author(s):  
Dmitry Gabrilovich ◽  
Tadao Ishida ◽  
Tsunehiro Oyama ◽  
Sophia Ran ◽  
Vladimir Kravtsov ◽  
...  
Keyword(s):  
Stem Cells ◽  
Vascular Endothelial Growth Factor ◽  
Dendritic Cells ◽  
Growth Factor ◽  
System Control ◽  
Vascular Endothelial ◽  
Almost All ◽  
Endothelial Growth Factor

Abstract Defective function of dendritic cells (DC) in cancer has been recently described and may represent one of the mechanisms of tumor evasion from immune system control. We have previously shown in vitro that vascular endothelial growth factor (VEGF), produced by almost all tumors, is one of the tumor-derived factors responsible for the defective function of these cells. In this study, we investigated whether in vivo infusion of recombinant VEGF could reproduce the observed DC dysfunction. Continuous VEGF infusion, at rates as low as 50 ng/h (resulting in serum VEGF concentrations of 120 to 160 pg/mL), resulted in a dramatic inhibition of dendritic cell development, associated with an increase in the production of B cells and immature Gr-1+ myeloid cells. Infusion of VEGF was associated with inhibition of the activity of the transcription factor NF-κB in bone marrow progenitor cells. Experiments in vitro showed that VEGF itself, and not factors released by VEGF-activated endothelial cells, affected polypotent stem cells resulting in the observed abnormal hematopoiesis. These data suggest that VEGF, at pathologically relevant concentrations in vivo, may exert effects on pluripotent stem cells that result in blocked DC development as well as affect many other hematopoietic lineages.

scholarly journals Up-regulation of Vascular Endothelial Growth Factor C in Breast Cancer Cells by Heregulin-β1

2002 ◽  
Vol 278 (8) ◽  
pp. 5750-5759 ◽  
Author(s):  
Pei-Wen Tsai ◽  
Shine-Gwo Shiah ◽  
Ming-Tsan Lin ◽  
Cheng-Wen Wu ◽  
Min-Liang Kuo
Keyword(s):  
Breast Cancer ◽  
Vascular Endothelial Growth Factor ◽  
Growth Factor ◽  
Cancer Cells ◽  
Breast Cancer Cells ◽  
Vascular Endothelial ◽  
Factor C ◽  
Endothelial Growth Factor
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