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           Search results for: Mouse Vascular Endothelial Growth Factor-165 VEGF-165   

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Anticancer effects of novel thalidomide analogs in A549 cells through inhibition of vascular endothelial growth factor and matrix metalloproteinase-2.

Lung cancer is one of the major causes of cancer-related mortality worldwide, and non-small-cell lung cancer is the most common form of lung cancer. Several studies had shown that thalidomide has potential for prevention and therapy of cancer. Therefore, the current study aimed to investigate the antitumor effects of two novel thalidomide analogs in human lung cancer A549 cells. The antiproliferative, antimigratory, and apoptotic effects in A549 cells induced by thalidomide analogs were examined. In addition, their effects on the expression of mRNAs encoding vascular endothelial growth factor165 (VEGF165) and matrix metalloproteinase-2 (MMP-2) were evaluated. Their influence on the tumor volume in nude mice was also determined. Results revealed that thalidomide analogs exhibited antiproliferative, antimigratory, and apoptotic activities with more pronounced effect than thalidomide drug. Furthermore, analogs 1 and 2 suppressed the expression levels of VEGF165 by 42% and 53.2% and those of MMP-2 by 45% and 52%, respectively. Thalidomide analogs 1 and 2 also reduced the tumor volume by 30.11% and 53.52%, respectively. Therefore, this study provides evidence that thalidomide analogs may serve as a new therapeutic option for treating lung cancer.

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Human Endocrine Gland Vas Human Vascular Endothelia Human Vascular Endothelia Mouse Vascular Endothelia Mouse Vascular Endothelia Rat Vascular Endothelial Mouse Vascular Endothelia Recombinant Human Vascula Epidermal Growth Factor ( Epidermal Growth Factor ( Human Insulin-like Growth Human Insulin-like Growth

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Bovine lactoferricin inhibits basic fibroblast growth factor- and vascular endothelial growth factor165-induced angiogenesis by competing for heparin-like binding sites on endothelial cells.

Angiogenesis is a complex process whereby new blood vessels form from pre-existing vasculature in response to proangiogenic factors such as basic fibroblast growth factor (bFGF) and the 165-kd isoform of vascular endothelial growth factor (VEGF165). Angiogenesis inhibitors show considerable potential in the treatment of cancer because angiogenesis is necessary for tumor growth beyond a few millimeters in diameter because of the tumor's need for oxygen and nutrient supply, as well as waste removal. Bovine lactoferricin (LfcinB) is a peptide fragment of iron- and heparin-binding lactoferrin obtained from cow's milk. Here we provide in vivo and in vitro evidence that LfcinB has potent antiangiogenic activity. LfcinB strongly inhibited both bFGF- and VEGF165-induced angiogenesis in Matrigel plugs implanted in C57BL/6 mice. In addition, LfcinB inhibited the in vitro proliferation and migration of human umbilical vein endothelial cells (HUVECs) in response to bFGF or VEGF165 but was not cytotoxic to HUVECs. Rather, LfcinB complexed with heparin-like structures on the HUVEC surface that are involved in the binding of bFGF and VEGF165 to their respective receptors, thereby preventing receptor-stimulated angiogenesis. These findings suggest that LfcinB may have utility as an antiangiogenic agent for the treatment of human cancers.

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Human Endocrine Gland Vas Human Vascular Endothelia Human Vascular Endothelia Mouse Vascular Endothelia Mouse Vascular Endothelia Rat Vascular Endothelial Mouse Vascular Endothelia Recombinant Human Vascula Human Fibroblast Growth F Human Fibroblast Growth F Mouse Fibroblast Growth F Recombinant Human Fibrobl

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[Experimental studies on inhibition of malignant melanoma growth by gene transfer of adenovirus-mediated averse vascular endothelial growth factor165].

To investigate the effect of Adenovirus-mediated averse vascular endothelial growth factor165(Ad-aVEGF165)on the growth of human melanoma cells(A375) in vivo and in vitro.

1460 related Products with: [Experimental studies on inhibition of malignant melanoma growth by gene transfer of adenovirus-mediated averse vascular endothelial growth factor165].

Human Endocrine Gland Vas Human Vascular Endothelia Human Vascular Endothelia Mouse Vascular Endothelia Mouse Vascular Endothelia Rat Vascular Endothelial Mouse Vascular Endothelia Recombinant Human Vascula Mouse Anti-Insulin-Like G Borellia grade BSA powde Borellia grade BSA powde Borellia grade BSA powde

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VEGF165 antisense RNA suppresses oncogenic properties of human esophageal squamous cell carcinoma.

To investigate the effect of antisense RNA to vascular endothelial growth factor165 (VEGF165) on human esophageal squamous cell carcinoma cell line EC109 and the feasibility of gene therapy for esophageal carcinoma.

1003 related Products with: VEGF165 antisense RNA suppresses oncogenic properties of human esophageal squamous cell carcinoma.

Human Squamous Cell Carci Human squamous cell carci Esophageal squamous cell Esophageal squamous cell Esophageal squamous cell Esophageal squamous cell Multiple organ squamous c Esophagus squamous cell c Esophagus squamous cell c Lung squamous cell carcin Skin malignant tumor tiss Head and neck squamous ce

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Neovasculature induced by vascular endothelial growth factor is fenestrated.

We have reported previously that topical administration of vascular endothelial growth factor165 (VEGF) to a microvascular bed supplied with a continuous endothelium can rapidly induce the formation of endothelial fenestrations (W. G. Roberts and G. E. Palade, J. Cell Sci., 108: 2369-2379, 1995). From these results, we hypothesized that tumor vasculature, in general, may also be fenestrated because it has been reported that tumor secretion of VEGF causes the surrounding host vasculature to invade and feed the growing tumor. Using electron microscopy to characterize the endothelial cell morphology in tumor vessels from either the periphery or the core of the tumor and immunoblotting to detect secreted VEGF, we analyzed the vasculature of human and murine neoplastic tumors grown s.c. in male nude mice. To clarify the role of VEGF165 two models were used: (a) Chinese hamster ovary (CHO) cells stably transfected with hu VEGF165 and injected into mice (VEGF:CHO tumors); and (b) slow-release pellets containing purified VEGF or basic fibroblast growth factor implanted on the rat cremaster muscle. All tumors had vessels with fenestrated endothelium, open interendothelial junctions, and clustered fused caveolae. From all of the peripheral tumor vessels observed, fenestrated endothelium was observed in 41% from EMT, 35% from M1S, 37% from U87, and 56% from VEGF:CHO tumors, whereas surrounding skin and muscle, from which tumor vessels were derived, had fenestrated endothelium in 2 and 0% of all vessels, respectively. Additionally, further analysis revealed a substantial decrease in the anionic glycocalyx on the luminal face of the fenestral diaphragms in endothelium from tumors (especially VEGF:CHO) when compared to intestine or pancreas. Because the host tissue microvascular endothelium which supplies the tumor is not fenestrated, tumors can transform nonproliferating, nonfenestrated vessels into proliferating vessels, many of which have fenestrated endothelium. These data provide evidence that chronic VEGF exposure can induce fenestrations in nonfenestrated endothelium similar to the fenestrated endothelium found in tumor vessels.

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