scholarly journals Vascular endothelial growth factor receptor-3 promotes breast cancer cell proliferation, motility and survival in vitro and tumor formation in vivo

Cell Cycle ◽  
2009 ◽  
Vol 8 (14) ◽  
pp. 2266-2280 ◽  
Author(s):  
Elena V. Kurenova ◽  
Darrell L. Hunt ◽  
Dihua He ◽  
Ann D. Fu ◽  
Nicole A. Massoll ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Vascular Endothelial Growth Factor ◽  
Growth Factor Receptor ◽  
Tumor Formation ◽  
Vascular Endothelial ◽  
Cancer Cell Proliferation ◽  
Breast Cancer Cell Proliferation ◽  
Endothelial Growth Factor

scholarly journals Analysis of Plant-derived Phytochemicals as Anti-cancer Agents Targeting Cyclin Dependent Kinase-2, Human Topoisomerase IIa and Vascular Endothelial Growth Factor Receptor-2

2020 ◽  
Author(s):  
Bishajit Sarkar ◽  
Md. Asad Ullah ◽  
Syed Sajidul Islam ◽  
Md. Hasanur Rahman
Keyword(s):  
Vascular Endothelial Growth Factor ◽  
Growth Factor ◽  
Growth Factor Receptor ◽  
Vascular Endothelial ◽  
Cyclin Dependent Kinase ◽  
Molecular Docking Study ◽  
Topoisomerase Iiα ◽  
Endothelial Growth Factor

AbstractCancer is caused by a variety of pathways, involving numerous types of enzymes, among them three enzymes: Cyclin dependent kinase-2 (CDK-2), Human topoisomerase IIα and Vascular Endothelial Growth Factor Receptor-2 (VEGFR-2) are three most common enzymes that are involved in the cancer development. Although many chemical drugs are available in the market, plant sources are known to contain a wide variety of agents that are known to possess anticancer activity. In this experiment, total thirty compounds were analysed against the mentioned enzymes using different tools of bioinformatics and in silico biology like molecular docking study, druglikeness property experiment, ADME/T test, PASS prediction and P450 site of metabolism prediction as well as DFT calculations to determine three best ligands that have the capability to inhibit the mentioned enzymes. Form the experiment, Epigallocatechin gallate was found to be the best ligand to inhibit CDK-2, Daidzein showed best inhibitory activities towards Human topoisomerase IIα and Quercetin was predicted to be the best agent against VEGFR-2. They were also predicted to be quite safe and effective agents to treat cancer. However, more in vivo and in vitro analysis are required to confirm their safety and efficacy in this regard.

A highly selective, orally bioavailable, vascular endothelial growth factor receptor-2 tyrosine kinase inhibitor has potent activity in vitro and in vivo

Angiogenesis ◽  
2009 ◽  
Vol 12 (3) ◽  
pp. 287-296 ◽  
Author(s):  
Kenneth R. LaMontagne ◽  
Jeannene Butler ◽  
Virna B. Borowski ◽  
Angel R. Fuentes-Pesquera ◽  
Jonathan M. Blevitt ◽  
...  
Keyword(s):  
Vascular Endothelial Growth Factor ◽  
Growth Factor ◽  
Tyrosine Kinase Inhibitor ◽  
Kinase Inhibitor ◽  
Growth Factor Receptor ◽  
Vascular Endothelial ◽  
Orally Bioavailable ◽  
Endothelial Growth Factor

scholarly journals Anti-cancer effects of F16: A novel vascular endothelial growth factor receptor–specific inhibitor

Tumor Biology ◽  
2017 ◽  
Vol 39 (11) ◽  
pp. 101042831772684 ◽  
Author(s):  
Appu Rathinavelu ◽  
Khalid Alhazzani ◽  
Sivanesan Dhandayuthapani ◽  
Thanigaivelan Kanagasabai
Keyword(s):  
Vascular Endothelial Growth Factor ◽  
Growth Factor ◽  
Tumor Growth ◽  
Growth Factor Receptor ◽  
Specific Inhibitor ◽  
Vascular Endothelial ◽  
And Migration ◽  
Endothelial Growth Factor

Vascular endothelial growth factor receptor-2 is a dynamic target for therapeutic intervention in various types of cancers. This study was aimed to explore the anti-angiogenic activity of a novel vascular endothelial growth factor receptor–specific inhibitor named F16 in both in vitro and in vivo experimental models. This compound effectively reduced cell proliferation, tube formation, and migration of human umbilical vein endothelial cells in a concentration-dependent manner by directly inhibiting vascular endothelial growth factor binding and subsequent vascular endothelial growth factor receptor-2 phosphorylation. The F16 was also able to inhibit the phosphoinositide 3-kinase/protein kinase B–mediated survival and migration pathways in cancer in addition to inhibiting the focal adhesion kinase and mitogen-activated protein kinases–mediated signaling in GI-101A cancer cells. The chorioallantoic membrane assay followed by tumor growth inhibition measurements with GI-101A breast cancer xenograft implanted athymic nude mice confirmed the in vivo tumor reductive effects of F16. It was interesting to observe a decrease in tumor burden after F16 treatment which correlated very well with the decrease in the plasma levels of mucin-1 (MUC-1). Our studies so far have confirmed that F16 is a specific inhibitor of angiogenesis in both in vitro and in vivo models. The F16 also works very efficiently with Taxol in combination by limiting the tumor growth that is better than the monotherapy with any one of the drugs that were tested individually. Thus, F16 offers a promising anti-proliferative and anti-angiogenic effects with better specificity than some of the existing multi-kinase inhibitors.

scholarly journals Estrogen regulation of vascular endothelial growth factor in breast cancer in vitro and in vivo: the role of estrogen receptor α and c-Myc

2009 ◽  
Vol 16 (3) ◽  
pp. 819-834 ◽  
Author(s):  
Maya Dadiani ◽  
Dalia Seger ◽  
Tamar Kreizman ◽  
Daria Badikhi ◽  
Raanan Margalit ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Vascular Endothelial Growth Factor ◽  
Estrogen Receptor Α ◽  
Vascular Endothelial ◽  
Estrogen Regulation ◽  
Endothelial Growth Factor

The role of c-Myc in estrogen regulation of vascular endothelial growth factor (VEGF) and of the vasculature function has been investigated in breast cancer cells and tumors. The studies were performed on MCF7 wild-type cells and MCF7-35im clone, stably transfected with an inducible c-Myc gene. In vitro and ex vivo methods for investigating molecular events were integrated with in vivo magnetic resonance imaging of the vascular function. The results showed that the c-Myc upregulation by estrogen is necessary for the transient induction of VEGF transcription; however, overexpression of c-Myc alone is not sufficient for this induction. Furthermore, both c-Myc and the activated estrogen receptor α (ERα) were shown to co-bind the VEGF promoter in close proximity, indicating a novel mechanism for estrogen regulation of VEGF. Studies of long-term estrogen treatment and overexpression of c-Myc alone demonstrated regulation of stable VEGF expression levels in vitro and in vivo, maintaining steady vascular permeability in tumors. However, withdrawal of estrogen from the tumors resulted in increased VEGF and elevated vascular permeability, presumably due to hypoxic conditions that were found to dominate VEGF overexpression in cultured cells. This work revealed a cooperative role for ERα and c-Myc in estrogen regulation of VEGF and the ability of c-Myc to partially mimic estrogen regulation of angiogenesis. It also illuminated the differences in estrogen regulation of VEGF during transient and long-term sustained treatments and under different microenvironmental conditions, providing a complementary picture of the in vitro and in vivo results.

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