scholarly journals Inhibition of Akt (ser473) Phosphorylation and Rapamycin-Resistant Cell Growth by Knockdown of Mammalian Target of Rapamycin with Small Interfering RNA in Vascular Endothelial Growth Factor Receptor-1-Targeting Vector

2011 ◽  
Vol 34 (5) ◽  
pp. 602-608 ◽  
Author(s):  
Hiroyuki Koide ◽  
Tomohiro Asai ◽  
Keiichi Furuya ◽  
Takuma Tsuzuku ◽  
Hiroki Kato ◽  
...  
Keyword(s):  
Vascular Endothelial Growth Factor ◽  
Growth Factor ◽  
Small Interfering Rna ◽  
Mammalian Target Of Rapamycin ◽  
Growth Factor Receptor ◽  
Resistant Cell ◽  
Vascular Endothelial ◽  
Targeting Vector ◽  
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.

Quelle stratégie thérapeutique pour les stades métastatiques ?

ONCOLOGIE ◽  
2018 ◽  
Vol 20 (7-12) ◽  
pp. 211-219
Author(s):  
A. Simonaggio ◽  
G. Rivallin ◽  
S. Marret ◽  
S. Oudard ◽  
Y.-A. Vano
Keyword(s):  
Vascular Endothelial Growth Factor ◽  
Growth Factor ◽  
Tyrosine Kinase ◽  
Mammalian Target Of Rapamycin ◽  
Growth Factor Receptor ◽  
Prise En Charge ◽  
Vascular Endothelial ◽  
Stratégie Thérapeutique ◽  
Inhibiteurs De Tyrosine Kinase ◽  
Endothelial Growth Factor

La prise en charge thérapeutique des carcinomes rénaux métastatiques à cellules claires a progressé de manière majeure sur la dernière décennie avec l’émergence des antiangiogéniques et inhibiteurs de mammalian target of rapamycin. Récemment, deux nouvelles molécules ont été validées et sont remboursées en France en deuxième ligne : nivolumab et cabozantinib. La première ligne connaît elle aussi de profonds changements avec l’approbation imminente de la combinaison nivolumab–ipilimumab pour les patients de pronostic intermédiaire à mauvais et les premiers résultats de l’association atézolizumab–bévacizumab qui pourrait se positionner en première ligne pour les patients exprimant PD-L1 et/ou de pronostic favorable. D’autres études de combinaison (inhibiteurs de tyrosine-kinase du vascular endothelial growth factor receptor–inhibiteurs des checkpoints immunitaires) sont en cours. La stratégie est également bouleversée chez les patients d’emblée métastatiques puisque l’étude CARMENA remet en cause la place de la néphrectomie chez ces patients. L’enjeu est donc de définir la meilleure séquence thérapeutique pour chaque patient, tout en s’adaptant régulièrement aux nouvelles données.

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