Neutralizing vascular endothelial growth factor activity inhibits thyroid cancer growth in vivo

Surgery ◽  
2000 ◽  
Vol 128 (6) ◽  
pp. 1059-1066 ◽  
Author(s):  
Euy Y. Soh ◽  
Monica S. Eigelberger ◽  
K.Jin Kim ◽  
Mariwil G. Wong ◽  
David M. Young ◽  
...  
Keyword(s):  
Vascular Endothelial Growth Factor ◽  
Thyroid Cancer ◽  
Growth Factor ◽  
Cancer Growth ◽  
Vascular Endothelial ◽  
Factor Activity ◽  
Endothelial Growth Factor

Neutralizing vascular endothelial growth factor activity inhibits thyroid cancer growth in vivo

2000 ◽  
Vol 87 (9) ◽  
pp. 1275-1276
Author(s):  
E. Y. Soh ◽  
K. J. Kim ◽  
M. S. Eigelberger ◽  
M. G. Wong ◽  
Q.-Y. Duh ◽  
...  
Keyword(s):  
Vascular Endothelial Growth Factor ◽  
Thyroid Cancer ◽  
Growth Factor ◽  
Cancer Growth ◽  
Vascular Endothelial ◽  
Factor Activity ◽  
Endothelial Growth Factor

scholarly journals Role of vascular endothelial growth factor in inducing production of angiopoetin-1 – in vivo study in Fisher rats

2017 ◽  
Vol 68 (4) ◽  
pp. 326-329
Author(s):  
Piotr Barć ◽  
Tomasz Płonek ◽  
Dagmara Baczyńska ◽  
Artur Pupka ◽  
Wojciech Witkiewicz ◽  
...  
Keyword(s):  
Vascular Endothelial Growth Factor ◽  
Growth Factor ◽  
In Vivo Study ◽  
Vascular Endothelial ◽  
Angiopoetin 1 ◽  
Endothelial Growth Factor

Glipizide Combined with ANP Suppresses Breast Cancer Growth and Metastasis by Inhibiting Angiogenesis through VEGF/VEGFR2 Signaling

2021 ◽  
Vol 21 ◽  
Author(s):  
Guanquan Mao ◽  
Shuting Zheng ◽  
Jinlian Li ◽  
Xiaohua Liu ◽  
Qin Zhou ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Vascular Endothelial Growth Factor ◽  
Growth Factor ◽  
Natriuretic Peptide ◽  
Umbilical Vein ◽  
Tube Formation ◽  
Cancer Growth ◽  
Vascular Endothelial ◽  
Breast Cancer Growth ◽  
Endothelial Growth Factor

Background: Breast cancer is one of the most common cancers worldwide among women, and angiogenesis has an important effect on its growth and metastasis. Glipizide, which is a widely used drug for type 2 diabetes mellitus, has been reported to inhibit tumor growth and metastasis by upregulating the expression of natriuretic peptide receptor A (NPRA). Atrial natriuretic peptide (ANP), the receptor of NPRA, plays an important role in angiogenesis. The purpose of this study was to explore the effect of glipizide combined with ANP on breast cancer growth and metastasis. Methods: To investigate the effect of glipizide combined with ANP on breast cancer, glipizide, ANP or glipizide combined with ANP was intraperitoneally injected into MMTV-PyMT mice. To explore whether the anticancer efficacy of glipizide combined with ANP was correlated with angiogenesis, a tube formation assay was performed. Results: Glipizide combined with ANP was found to inhibit breast cancer growth and metastasis in MMTV-PyMT mice, which spontaneously develop breast cancer. Furthermore, the inhibitory effect of ANP combined with glipizide was better than that of glipizide alone. ANP combined with glipizide significantly inhibited tube formation of human umbilical vein endothelial cells (HUVECs) by suppressing vascular endothelial growth factor (VEGF)/VEGFR2 (vascular endothelial growth factor receptor 2) signaling. Conclusions: These results demonstrate that glipizide combined with ANP has a greater potential than glipizide alone to be repurposed as effective agents for the treatment of breast cancer by targeting tumor-induced angiogenesis.

Mice overexpressing placenta growth factor exhibit increased vascularization and vessel permeability

2002 ◽  
Vol 115 (12) ◽  
pp. 2559-2567 ◽  
Author(s):  
Teresa Odorisio ◽  
Cataldo Schietroma ◽  
M. Letizia Zaccaria ◽  
Francesca Cianfarani ◽  
Cecilia Tiveron ◽  
...  
Keyword(s):  
Vascular Endothelial Growth Factor ◽  
Growth Factor ◽  
Adult Life ◽  
Growth Factor Receptor ◽  
Vascular Endothelial ◽  
Placenta Growth Factor ◽  
Vessel Permeability ◽  
Exact Function ◽  
Endothelial Growth Factor

Placenta growth factor (PlGF) is a member of the vascular endothelial growth factor (VEGF) family, comprising at least five cytokines specifically involved in the regulation of vascular and/or lymphatic endothelium differentiation. Several lines of evidence indicate a role for PlGF in monocyte chemotaxis and in potentiating the activity of VEGF, but the exact function of this cytokine is not fully understood. To define the biological role of PlGF in vivo, we have produced a transgenic mouse model overexpressing this factor in the skin by using a keratin 14 promoter cassette. Our data indicate that PlGF has strong angiogenic properties in both fetal and adult life. PlGF overexpression results in a substantial increase in the number,branching and size of dermal blood vessels as well as in enhanced vascular permeability. Indeed, intradermally injected recombinant PlGF was able to induce vessel permeability in wild-type mice. The analysis of vascular endothelial growth factor receptor 1/flt-1 and vascular endothelial growth factor receptor 2/flk-1 indicates that the two receptors are induced in the skin endothelium of transgenic mice suggesting that both are involved in mediating the effect of overexpressed PlGF.

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