scholarly journals A small interfering RNA targeting vascular endothelial growth factor efficiently inhibits growth of VX2 cells and VX2 tumor model of hepatocellular carcinoma in rabbit by transarterial embolization-mediated siRNA delivery

2016 ◽  
pp. 1243 ◽  
Author(s):  
Yu Zou ◽  
Cai-Yun Fu ◽  
Chuan-Gen Guo ◽  
Zhen-Gang Yang ◽  
Jun-Hui Sun ◽  
...  
Keyword(s):  
Hepatocellular Carcinoma ◽  
Small Interfering Rna ◽  
Transarterial Embolization ◽  
Sirna Delivery ◽  
Tumor Model ◽  
Vascular Endothelial ◽  
Rna Targeting ◽  
Vx2 Tumor ◽  
Interfering Rna ◽  
Endothelial Growth Factor

scholarly journals A Small Interfering RNA Targeting Vascular Endothelial Growth Factor as Cancer Therapeutics

2004 ◽  
Vol 64 (10) ◽  
pp. 3365-3370 ◽  
Author(s):  
Yoshifumi Takei ◽  
Kenji Kadomatsu ◽  
Yukio Yuzawa ◽  
Seiichi Matsuo ◽  
Takashi Muramatsu
Keyword(s):  
Vascular Endothelial Growth Factor ◽  
Growth Factor ◽  
Small Interfering Rna ◽  
Cancer Therapeutics ◽  
Vascular Endothelial ◽  
Rna Targeting ◽  
Interfering Rna ◽  
Endothelial Growth Factor

scholarly journals Vascular Endothelial Growth Factor-A (VEGF-A) Mediates Activin A-Induced Human Trophoblast Endothelial-Like Tube Formation

Endocrinology ◽  
2015 ◽  
Vol 156 (11) ◽  
pp. 4257-4268 ◽  
Author(s):  
Yan Li ◽  
Hua Zhu ◽  
Christian Klausen ◽  
Bo Peng ◽  
Peter C. K. Leung
Keyword(s):  
Vascular Endothelial Growth Factor ◽  
Growth Factor ◽  
Small Interfering Rna ◽  
Activin A ◽  
Tube Formation ◽  
Dependent Manner ◽  
Vascular Endothelial ◽  
Human Trophoblast ◽  
Interfering Rna ◽  
Endothelial Growth Factor

Remodeling of maternal spiral arteries during pregnancy requires a subpopulation of extravillous cytotrophoblasts (EVTs) to differentiate into endovascular EVTs. Activin A, which is abundantly expressed at the maternal-fetal interface, has been shown to promote trophoblast invasion, but its role in endovascular differentiation remains unknown. Vascular endothelial growth factor-A (VEGF-A) is well recognized as a key regulator in trophoblast endovascular differentiation. Whether and how activin A might regulate VEGF-A production in human trophoblasts and its relationship to endovascular differentiation have yet to be determined. In the present study, we found that activin A increased VEGF-A production in primary and immortalized (HTR8/SVneo) human EVT cells. In addition, activin A enhanced HTR8/SVneo endothelial-like tube formation, and these effects were attenuated by pretreatment with small interfering RNA targeting VEGF-A or the VEGF receptor 1/2 inhibitor SU4312. Pretreatment with the activin/TGF-β type 1 receptor (ALK4/5/7) inhibitor SB431542 abolished the stimulatory effects of activin A on phosphorylated mothers against decapentaplegic (SMAD)-2/3 phosphorylation, VEGF-A production, and endothelial-like tube formation. Moreover, small interfering RNA-mediated down-regulation of SMAD2, SMAD3, or common SMAD4 abolished the effects of activin A on VEGF-A production and endothelial-like tube formation. In conclusion, activin A may promote human trophoblast cell endothelial-like tube formation by up-regulating VEGF-A production in an SMAD2/3-SMAD4-dependent manner. These findings provide insight into the cellular and molecular events regulated by activin A during human implantation.

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