human umbilical cord endothelial cells huvecs Search Results


human umbilical vein endothelial cells  (ATCC)
95
ATCC human umbilical vein endothelial cells
Human Umbilical Vein Endothelial Cells, supplied by ATCC, used in various techniques. Bioz Stars score: 95/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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human umbilical vascular endothelial cells huvec  (Cell Applications Inc)
95
Cell Applications Inc human umbilical vascular endothelial cells huvec
Fig. 5. Cyclic 7-mer peptides bind NRP1and inhibit CL1-5 invasion and angiogenesis in vivo. A, the selected peptides reduce phosphorylation ofVEGFR2. <t>HUVECs</t> were pretreated with peptides for10 min followed by treatment withVEGF for 5 min. Phosphorylation ofVEGFR2 was determined byWestern blotting with an anti ^ phospho-VEGFR2 antibody.TotalVEGFR2 was determined byWestern blotting with an anti-VEGFR2 antibody. B, the effect of peptides on CL1-5 cells invasive activity. The invasive activity of cells was detected by invasion assay. CL1-5 cells (2.5 104) were seeded onTranswells coated with 30 Ag matrigel and incubated with peptides DG1or DG2 for 48 h.Then, the cells that had invaded the membrane were counted.Values were normalized to the relative invasion activity of the nontreated control cells. Experiments were done in triplicate, three independent times. In DG1- and DG2-treated cells, the invasion ability was statistically significantly different across the various concentrations of DG1or DG2 byANOVA (DG1, P < 0.001; DG2, P = 0.011). C, the effect of peptides on tumor angiogenesis in vivo. Immunohistochemical staining of the Matrigel plug sections with an anti-CD31antibody showed a significant decrease in CD31-positive vessels in plugs containing DG1peptide compared with mock-treated plugs. Original magnification, 200.The counts of microvessels surrounding the tumor nests were calculated. D, effect of peptides on tumorigenesis in vivo.Volumes of tumors from control CL1-5 cells (E) and DG1-treated cells (n) were measured at the indicated times as described in Materials and Methods. Means and 95% CI are shown (n = 5 mice per group). E, summary diagram showing thatVEGF165 can bind to NRP1and trigger the NRP1/VEGFR2/PI3K/Akt signaling pathways and result in tumor angiogenesis, cancer cell invasion, and tumorigenesis.The synthetic peptides DG1/DG2 can specifically block this signaling pathway and may have therapeutic potential.
Human Umbilical Vascular Endothelial Cells Huvec, supplied by Cell Applications Inc, used in various techniques. Bioz Stars score: 95/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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human umbilical vein endothelial cells  (Lonza)
99
Lonza human umbilical vein endothelial cells
Fig. 5. Cyclic 7-mer peptides bind NRP1and inhibit CL1-5 invasion and angiogenesis in vivo. A, the selected peptides reduce phosphorylation ofVEGFR2. <t>HUVECs</t> were pretreated with peptides for10 min followed by treatment withVEGF for 5 min. Phosphorylation ofVEGFR2 was determined byWestern blotting with an anti ^ phospho-VEGFR2 antibody.TotalVEGFR2 was determined byWestern blotting with an anti-VEGFR2 antibody. B, the effect of peptides on CL1-5 cells invasive activity. The invasive activity of cells was detected by invasion assay. CL1-5 cells (2.5 104) were seeded onTranswells coated with 30 Ag matrigel and incubated with peptides DG1or DG2 for 48 h.Then, the cells that had invaded the membrane were counted.Values were normalized to the relative invasion activity of the nontreated control cells. Experiments were done in triplicate, three independent times. In DG1- and DG2-treated cells, the invasion ability was statistically significantly different across the various concentrations of DG1or DG2 byANOVA (DG1, P < 0.001; DG2, P = 0.011). C, the effect of peptides on tumor angiogenesis in vivo. Immunohistochemical staining of the Matrigel plug sections with an anti-CD31antibody showed a significant decrease in CD31-positive vessels in plugs containing DG1peptide compared with mock-treated plugs. Original magnification, 200.The counts of microvessels surrounding the tumor nests were calculated. D, effect of peptides on tumorigenesis in vivo.Volumes of tumors from control CL1-5 cells (E) and DG1-treated cells (n) were measured at the indicated times as described in Materials and Methods. Means and 95% CI are shown (n = 5 mice per group). E, summary diagram showing thatVEGF165 can bind to NRP1and trigger the NRP1/VEGFR2/PI3K/Akt signaling pathways and result in tumor angiogenesis, cancer cell invasion, and tumorigenesis.The synthetic peptides DG1/DG2 can specifically block this signaling pathway and may have therapeutic potential.
Human Umbilical Vein Endothelial Cells, supplied by Lonza, used in various techniques. Bioz Stars score: 99/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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cells huvecs  (Angio-Proteomie)
92
Angio-Proteomie cells huvecs
Fig. 5. Cyclic 7-mer peptides bind NRP1and inhibit CL1-5 invasion and angiogenesis in vivo. A, the selected peptides reduce phosphorylation ofVEGFR2. <t>HUVECs</t> were pretreated with peptides for10 min followed by treatment withVEGF for 5 min. Phosphorylation ofVEGFR2 was determined byWestern blotting with an anti ^ phospho-VEGFR2 antibody.TotalVEGFR2 was determined byWestern blotting with an anti-VEGFR2 antibody. B, the effect of peptides on CL1-5 cells invasive activity. The invasive activity of cells was detected by invasion assay. CL1-5 cells (2.5 104) were seeded onTranswells coated with 30 Ag matrigel and incubated with peptides DG1or DG2 for 48 h.Then, the cells that had invaded the membrane were counted.Values were normalized to the relative invasion activity of the nontreated control cells. Experiments were done in triplicate, three independent times. In DG1- and DG2-treated cells, the invasion ability was statistically significantly different across the various concentrations of DG1or DG2 byANOVA (DG1, P < 0.001; DG2, P = 0.011). C, the effect of peptides on tumor angiogenesis in vivo. Immunohistochemical staining of the Matrigel plug sections with an anti-CD31antibody showed a significant decrease in CD31-positive vessels in plugs containing DG1peptide compared with mock-treated plugs. Original magnification, 200.The counts of microvessels surrounding the tumor nests were calculated. D, effect of peptides on tumorigenesis in vivo.Volumes of tumors from control CL1-5 cells (E) and DG1-treated cells (n) were measured at the indicated times as described in Materials and Methods. Means and 95% CI are shown (n = 5 mice per group). E, summary diagram showing thatVEGF165 can bind to NRP1and trigger the NRP1/VEGFR2/PI3K/Akt signaling pathways and result in tumor angiogenesis, cancer cell invasion, and tumorigenesis.The synthetic peptides DG1/DG2 can specifically block this signaling pathway and may have therapeutic potential.
Cells Huvecs, supplied by Angio-Proteomie, used in various techniques. Bioz Stars score: 92/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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human umbilical vein  (Cell Applications Inc)
92
Cell Applications Inc human umbilical vein
Fig. 5. Cyclic 7-mer peptides bind NRP1and inhibit CL1-5 invasion and angiogenesis in vivo. A, the selected peptides reduce phosphorylation ofVEGFR2. <t>HUVECs</t> were pretreated with peptides for10 min followed by treatment withVEGF for 5 min. Phosphorylation ofVEGFR2 was determined byWestern blotting with an anti ^ phospho-VEGFR2 antibody.TotalVEGFR2 was determined byWestern blotting with an anti-VEGFR2 antibody. B, the effect of peptides on CL1-5 cells invasive activity. The invasive activity of cells was detected by invasion assay. CL1-5 cells (2.5 104) were seeded onTranswells coated with 30 Ag matrigel and incubated with peptides DG1or DG2 for 48 h.Then, the cells that had invaded the membrane were counted.Values were normalized to the relative invasion activity of the nontreated control cells. Experiments were done in triplicate, three independent times. In DG1- and DG2-treated cells, the invasion ability was statistically significantly different across the various concentrations of DG1or DG2 byANOVA (DG1, P < 0.001; DG2, P = 0.011). C, the effect of peptides on tumor angiogenesis in vivo. Immunohistochemical staining of the Matrigel plug sections with an anti-CD31antibody showed a significant decrease in CD31-positive vessels in plugs containing DG1peptide compared with mock-treated plugs. Original magnification, 200.The counts of microvessels surrounding the tumor nests were calculated. D, effect of peptides on tumorigenesis in vivo.Volumes of tumors from control CL1-5 cells (E) and DG1-treated cells (n) were measured at the indicated times as described in Materials and Methods. Means and 95% CI are shown (n = 5 mice per group). E, summary diagram showing thatVEGF165 can bind to NRP1and trigger the NRP1/VEGFR2/PI3K/Akt signaling pathways and result in tumor angiogenesis, cancer cell invasion, and tumorigenesis.The synthetic peptides DG1/DG2 can specifically block this signaling pathway and may have therapeutic potential.
Human Umbilical Vein, supplied by Cell Applications Inc, used in various techniques. Bioz Stars score: 92/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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human umbilical vein endothelial cells huvec passages 3–10  (Lonza)
90
Lonza human umbilical vein endothelial cells huvec passages 3–10
Fig. 5. Cyclic 7-mer peptides bind NRP1and inhibit CL1-5 invasion and angiogenesis in vivo. A, the selected peptides reduce phosphorylation ofVEGFR2. <t>HUVECs</t> were pretreated with peptides for10 min followed by treatment withVEGF for 5 min. Phosphorylation ofVEGFR2 was determined byWestern blotting with an anti ^ phospho-VEGFR2 antibody.TotalVEGFR2 was determined byWestern blotting with an anti-VEGFR2 antibody. B, the effect of peptides on CL1-5 cells invasive activity. The invasive activity of cells was detected by invasion assay. CL1-5 cells (2.5 104) were seeded onTranswells coated with 30 Ag matrigel and incubated with peptides DG1or DG2 for 48 h.Then, the cells that had invaded the membrane were counted.Values were normalized to the relative invasion activity of the nontreated control cells. Experiments were done in triplicate, three independent times. In DG1- and DG2-treated cells, the invasion ability was statistically significantly different across the various concentrations of DG1or DG2 byANOVA (DG1, P < 0.001; DG2, P = 0.011). C, the effect of peptides on tumor angiogenesis in vivo. Immunohistochemical staining of the Matrigel plug sections with an anti-CD31antibody showed a significant decrease in CD31-positive vessels in plugs containing DG1peptide compared with mock-treated plugs. Original magnification, 200.The counts of microvessels surrounding the tumor nests were calculated. D, effect of peptides on tumorigenesis in vivo.Volumes of tumors from control CL1-5 cells (E) and DG1-treated cells (n) were measured at the indicated times as described in Materials and Methods. Means and 95% CI are shown (n = 5 mice per group). E, summary diagram showing thatVEGF165 can bind to NRP1and trigger the NRP1/VEGFR2/PI3K/Akt signaling pathways and result in tumor angiogenesis, cancer cell invasion, and tumorigenesis.The synthetic peptides DG1/DG2 can specifically block this signaling pathway and may have therapeutic potential.
Human Umbilical Vein Endothelial Cells Huvec Passages 3–10, supplied by Lonza, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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human umbilical vein endothelial cells (huvec)  (Lonza)
90
Lonza human umbilical vein endothelial cells (huvec)
Fig. 5. Cyclic 7-mer peptides bind NRP1and inhibit CL1-5 invasion and angiogenesis in vivo. A, the selected peptides reduce phosphorylation ofVEGFR2. <t>HUVECs</t> were pretreated with peptides for10 min followed by treatment withVEGF for 5 min. Phosphorylation ofVEGFR2 was determined byWestern blotting with an anti ^ phospho-VEGFR2 antibody.TotalVEGFR2 was determined byWestern blotting with an anti-VEGFR2 antibody. B, the effect of peptides on CL1-5 cells invasive activity. The invasive activity of cells was detected by invasion assay. CL1-5 cells (2.5 104) were seeded onTranswells coated with 30 Ag matrigel and incubated with peptides DG1or DG2 for 48 h.Then, the cells that had invaded the membrane were counted.Values were normalized to the relative invasion activity of the nontreated control cells. Experiments were done in triplicate, three independent times. In DG1- and DG2-treated cells, the invasion ability was statistically significantly different across the various concentrations of DG1or DG2 byANOVA (DG1, P < 0.001; DG2, P = 0.011). C, the effect of peptides on tumor angiogenesis in vivo. Immunohistochemical staining of the Matrigel plug sections with an anti-CD31antibody showed a significant decrease in CD31-positive vessels in plugs containing DG1peptide compared with mock-treated plugs. Original magnification, 200.The counts of microvessels surrounding the tumor nests were calculated. D, effect of peptides on tumorigenesis in vivo.Volumes of tumors from control CL1-5 cells (E) and DG1-treated cells (n) were measured at the indicated times as described in Materials and Methods. Means and 95% CI are shown (n = 5 mice per group). E, summary diagram showing thatVEGF165 can bind to NRP1and trigger the NRP1/VEGFR2/PI3K/Akt signaling pathways and result in tumor angiogenesis, cancer cell invasion, and tumorigenesis.The synthetic peptides DG1/DG2 can specifically block this signaling pathway and may have therapeutic potential.
Human Umbilical Vein Endothelial Cells (Huvec), supplied by Lonza, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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human aortic endothelial cells (haecs)  (iCell Bioscience Inc)
90
iCell Bioscience Inc human aortic endothelial cells (haecs)
Fig. 5. Cyclic 7-mer peptides bind NRP1and inhibit CL1-5 invasion and angiogenesis in vivo. A, the selected peptides reduce phosphorylation ofVEGFR2. <t>HUVECs</t> were pretreated with peptides for10 min followed by treatment withVEGF for 5 min. Phosphorylation ofVEGFR2 was determined byWestern blotting with an anti ^ phospho-VEGFR2 antibody.TotalVEGFR2 was determined byWestern blotting with an anti-VEGFR2 antibody. B, the effect of peptides on CL1-5 cells invasive activity. The invasive activity of cells was detected by invasion assay. CL1-5 cells (2.5 104) were seeded onTranswells coated with 30 Ag matrigel and incubated with peptides DG1or DG2 for 48 h.Then, the cells that had invaded the membrane were counted.Values were normalized to the relative invasion activity of the nontreated control cells. Experiments were done in triplicate, three independent times. In DG1- and DG2-treated cells, the invasion ability was statistically significantly different across the various concentrations of DG1or DG2 byANOVA (DG1, P < 0.001; DG2, P = 0.011). C, the effect of peptides on tumor angiogenesis in vivo. Immunohistochemical staining of the Matrigel plug sections with an anti-CD31antibody showed a significant decrease in CD31-positive vessels in plugs containing DG1peptide compared with mock-treated plugs. Original magnification, 200.The counts of microvessels surrounding the tumor nests were calculated. D, effect of peptides on tumorigenesis in vivo.Volumes of tumors from control CL1-5 cells (E) and DG1-treated cells (n) were measured at the indicated times as described in Materials and Methods. Means and 95% CI are shown (n = 5 mice per group). E, summary diagram showing thatVEGF165 can bind to NRP1and trigger the NRP1/VEGFR2/PI3K/Akt signaling pathways and result in tumor angiogenesis, cancer cell invasion, and tumorigenesis.The synthetic peptides DG1/DG2 can specifically block this signaling pathway and may have therapeutic potential.
Human Aortic Endothelial Cells (Haecs), supplied by iCell Bioscience Inc, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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human umbilical vein endothelial cells (huvecs)  (Kurabo industries)
90
Kurabo industries human umbilical vein endothelial cells (huvecs)
Fig. 5. Cyclic 7-mer peptides bind NRP1and inhibit CL1-5 invasion and angiogenesis in vivo. A, the selected peptides reduce phosphorylation ofVEGFR2. <t>HUVECs</t> were pretreated with peptides for10 min followed by treatment withVEGF for 5 min. Phosphorylation ofVEGFR2 was determined byWestern blotting with an anti ^ phospho-VEGFR2 antibody.TotalVEGFR2 was determined byWestern blotting with an anti-VEGFR2 antibody. B, the effect of peptides on CL1-5 cells invasive activity. The invasive activity of cells was detected by invasion assay. CL1-5 cells (2.5 104) were seeded onTranswells coated with 30 Ag matrigel and incubated with peptides DG1or DG2 for 48 h.Then, the cells that had invaded the membrane were counted.Values were normalized to the relative invasion activity of the nontreated control cells. Experiments were done in triplicate, three independent times. In DG1- and DG2-treated cells, the invasion ability was statistically significantly different across the various concentrations of DG1or DG2 byANOVA (DG1, P < 0.001; DG2, P = 0.011). C, the effect of peptides on tumor angiogenesis in vivo. Immunohistochemical staining of the Matrigel plug sections with an anti-CD31antibody showed a significant decrease in CD31-positive vessels in plugs containing DG1peptide compared with mock-treated plugs. Original magnification, 200.The counts of microvessels surrounding the tumor nests were calculated. D, effect of peptides on tumorigenesis in vivo.Volumes of tumors from control CL1-5 cells (E) and DG1-treated cells (n) were measured at the indicated times as described in Materials and Methods. Means and 95% CI are shown (n = 5 mice per group). E, summary diagram showing thatVEGF165 can bind to NRP1and trigger the NRP1/VEGFR2/PI3K/Akt signaling pathways and result in tumor angiogenesis, cancer cell invasion, and tumorigenesis.The synthetic peptides DG1/DG2 can specifically block this signaling pathway and may have therapeutic potential.
Human Umbilical Vein Endothelial Cells (Huvecs), supplied by Kurabo industries, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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huvec (human umbilical vein endothelial cell)  (ScienCell)
90
ScienCell huvec (human umbilical vein endothelial cell)
Fig. 5. Cyclic 7-mer peptides bind NRP1and inhibit CL1-5 invasion and angiogenesis in vivo. A, the selected peptides reduce phosphorylation ofVEGFR2. <t>HUVECs</t> were pretreated with peptides for10 min followed by treatment withVEGF for 5 min. Phosphorylation ofVEGFR2 was determined byWestern blotting with an anti ^ phospho-VEGFR2 antibody.TotalVEGFR2 was determined byWestern blotting with an anti-VEGFR2 antibody. B, the effect of peptides on CL1-5 cells invasive activity. The invasive activity of cells was detected by invasion assay. CL1-5 cells (2.5 104) were seeded onTranswells coated with 30 Ag matrigel and incubated with peptides DG1or DG2 for 48 h.Then, the cells that had invaded the membrane were counted.Values were normalized to the relative invasion activity of the nontreated control cells. Experiments were done in triplicate, three independent times. In DG1- and DG2-treated cells, the invasion ability was statistically significantly different across the various concentrations of DG1or DG2 byANOVA (DG1, P < 0.001; DG2, P = 0.011). C, the effect of peptides on tumor angiogenesis in vivo. Immunohistochemical staining of the Matrigel plug sections with an anti-CD31antibody showed a significant decrease in CD31-positive vessels in plugs containing DG1peptide compared with mock-treated plugs. Original magnification, 200.The counts of microvessels surrounding the tumor nests were calculated. D, effect of peptides on tumorigenesis in vivo.Volumes of tumors from control CL1-5 cells (E) and DG1-treated cells (n) were measured at the indicated times as described in Materials and Methods. Means and 95% CI are shown (n = 5 mice per group). E, summary diagram showing thatVEGF165 can bind to NRP1and trigger the NRP1/VEGFR2/PI3K/Akt signaling pathways and result in tumor angiogenesis, cancer cell invasion, and tumorigenesis.The synthetic peptides DG1/DG2 can specifically block this signaling pathway and may have therapeutic potential.
Huvec (Human Umbilical Vein Endothelial Cell), supplied by ScienCell, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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human umbilical vein endothelial cells  (TCS Cellworks)
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TCS Cellworks human umbilical vein endothelial cells
Fig. 5. Cyclic 7-mer peptides bind NRP1and inhibit CL1-5 invasion and angiogenesis in vivo. A, the selected peptides reduce phosphorylation ofVEGFR2. <t>HUVECs</t> were pretreated with peptides for10 min followed by treatment withVEGF for 5 min. Phosphorylation ofVEGFR2 was determined byWestern blotting with an anti ^ phospho-VEGFR2 antibody.TotalVEGFR2 was determined byWestern blotting with an anti-VEGFR2 antibody. B, the effect of peptides on CL1-5 cells invasive activity. The invasive activity of cells was detected by invasion assay. CL1-5 cells (2.5 104) were seeded onTranswells coated with 30 Ag matrigel and incubated with peptides DG1or DG2 for 48 h.Then, the cells that had invaded the membrane were counted.Values were normalized to the relative invasion activity of the nontreated control cells. Experiments were done in triplicate, three independent times. In DG1- and DG2-treated cells, the invasion ability was statistically significantly different across the various concentrations of DG1or DG2 byANOVA (DG1, P < 0.001; DG2, P = 0.011). C, the effect of peptides on tumor angiogenesis in vivo. Immunohistochemical staining of the Matrigel plug sections with an anti-CD31antibody showed a significant decrease in CD31-positive vessels in plugs containing DG1peptide compared with mock-treated plugs. Original magnification, 200.The counts of microvessels surrounding the tumor nests were calculated. D, effect of peptides on tumorigenesis in vivo.Volumes of tumors from control CL1-5 cells (E) and DG1-treated cells (n) were measured at the indicated times as described in Materials and Methods. Means and 95% CI are shown (n = 5 mice per group). E, summary diagram showing thatVEGF165 can bind to NRP1and trigger the NRP1/VEGFR2/PI3K/Akt signaling pathways and result in tumor angiogenesis, cancer cell invasion, and tumorigenesis.The synthetic peptides DG1/DG2 can specifically block this signaling pathway and may have therapeutic potential.
Human Umbilical Vein Endothelial Cells, supplied by TCS Cellworks, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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human umbilical vein endothelial cells (huvecs, pelobiotech gmbh)  (PELOBIOTECH GmbH)
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PELOBIOTECH GmbH human umbilical vein endothelial cells (huvecs, pelobiotech gmbh)
Fig. 5. Cyclic 7-mer peptides bind NRP1and inhibit CL1-5 invasion and angiogenesis in vivo. A, the selected peptides reduce phosphorylation ofVEGFR2. <t>HUVECs</t> were pretreated with peptides for10 min followed by treatment withVEGF for 5 min. Phosphorylation ofVEGFR2 was determined byWestern blotting with an anti ^ phospho-VEGFR2 antibody.TotalVEGFR2 was determined byWestern blotting with an anti-VEGFR2 antibody. B, the effect of peptides on CL1-5 cells invasive activity. The invasive activity of cells was detected by invasion assay. CL1-5 cells (2.5 104) were seeded onTranswells coated with 30 Ag matrigel and incubated with peptides DG1or DG2 for 48 h.Then, the cells that had invaded the membrane were counted.Values were normalized to the relative invasion activity of the nontreated control cells. Experiments were done in triplicate, three independent times. In DG1- and DG2-treated cells, the invasion ability was statistically significantly different across the various concentrations of DG1or DG2 byANOVA (DG1, P < 0.001; DG2, P = 0.011). C, the effect of peptides on tumor angiogenesis in vivo. Immunohistochemical staining of the Matrigel plug sections with an anti-CD31antibody showed a significant decrease in CD31-positive vessels in plugs containing DG1peptide compared with mock-treated plugs. Original magnification, 200.The counts of microvessels surrounding the tumor nests were calculated. D, effect of peptides on tumorigenesis in vivo.Volumes of tumors from control CL1-5 cells (E) and DG1-treated cells (n) were measured at the indicated times as described in Materials and Methods. Means and 95% CI are shown (n = 5 mice per group). E, summary diagram showing thatVEGF165 can bind to NRP1and trigger the NRP1/VEGFR2/PI3K/Akt signaling pathways and result in tumor angiogenesis, cancer cell invasion, and tumorigenesis.The synthetic peptides DG1/DG2 can specifically block this signaling pathway and may have therapeutic potential.
Human Umbilical Vein Endothelial Cells (Huvecs, Pelobiotech Gmbh), supplied by PELOBIOTECH GmbH, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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Fig. 5. Cyclic 7-mer peptides bind NRP1and inhibit CL1-5 invasion and angiogenesis in vivo. A, the selected peptides reduce phosphorylation ofVEGFR2. HUVECs were pretreated with peptides for10 min followed by treatment withVEGF for 5 min. Phosphorylation ofVEGFR2 was determined byWestern blotting with an anti ^ phospho-VEGFR2 antibody.TotalVEGFR2 was determined byWestern blotting with an anti-VEGFR2 antibody. B, the effect of peptides on CL1-5 cells invasive activity. The invasive activity of cells was detected by invasion assay. CL1-5 cells (2.5 104) were seeded onTranswells coated with 30 Ag matrigel and incubated with peptides DG1or DG2 for 48 h.Then, the cells that had invaded the membrane were counted.Values were normalized to the relative invasion activity of the nontreated control cells. Experiments were done in triplicate, three independent times. In DG1- and DG2-treated cells, the invasion ability was statistically significantly different across the various concentrations of DG1or DG2 byANOVA (DG1, P < 0.001; DG2, P = 0.011). C, the effect of peptides on tumor angiogenesis in vivo. Immunohistochemical staining of the Matrigel plug sections with an anti-CD31antibody showed a significant decrease in CD31-positive vessels in plugs containing DG1peptide compared with mock-treated plugs. Original magnification, 200.The counts of microvessels surrounding the tumor nests were calculated. D, effect of peptides on tumorigenesis in vivo.Volumes of tumors from control CL1-5 cells (E) and DG1-treated cells (n) were measured at the indicated times as described in Materials and Methods. Means and 95% CI are shown (n = 5 mice per group). E, summary diagram showing thatVEGF165 can bind to NRP1and trigger the NRP1/VEGFR2/PI3K/Akt signaling pathways and result in tumor angiogenesis, cancer cell invasion, and tumorigenesis.The synthetic peptides DG1/DG2 can specifically block this signaling pathway and may have therapeutic potential.

Journal: Clinical Cancer Research

Article Title: Targeting Neuropilin 1 as an Antitumor Strategy in Lung Cancer

doi: 10.1158/1078-0432.ccr-07-0001

Figure Lengend Snippet: Fig. 5. Cyclic 7-mer peptides bind NRP1and inhibit CL1-5 invasion and angiogenesis in vivo. A, the selected peptides reduce phosphorylation ofVEGFR2. HUVECs were pretreated with peptides for10 min followed by treatment withVEGF for 5 min. Phosphorylation ofVEGFR2 was determined byWestern blotting with an anti ^ phospho-VEGFR2 antibody.TotalVEGFR2 was determined byWestern blotting with an anti-VEGFR2 antibody. B, the effect of peptides on CL1-5 cells invasive activity. The invasive activity of cells was detected by invasion assay. CL1-5 cells (2.5 104) were seeded onTranswells coated with 30 Ag matrigel and incubated with peptides DG1or DG2 for 48 h.Then, the cells that had invaded the membrane were counted.Values were normalized to the relative invasion activity of the nontreated control cells. Experiments were done in triplicate, three independent times. In DG1- and DG2-treated cells, the invasion ability was statistically significantly different across the various concentrations of DG1or DG2 byANOVA (DG1, P < 0.001; DG2, P = 0.011). C, the effect of peptides on tumor angiogenesis in vivo. Immunohistochemical staining of the Matrigel plug sections with an anti-CD31antibody showed a significant decrease in CD31-positive vessels in plugs containing DG1peptide compared with mock-treated plugs. Original magnification, 200.The counts of microvessels surrounding the tumor nests were calculated. D, effect of peptides on tumorigenesis in vivo.Volumes of tumors from control CL1-5 cells (E) and DG1-treated cells (n) were measured at the indicated times as described in Materials and Methods. Means and 95% CI are shown (n = 5 mice per group). E, summary diagram showing thatVEGF165 can bind to NRP1and trigger the NRP1/VEGFR2/PI3K/Akt signaling pathways and result in tumor angiogenesis, cancer cell invasion, and tumorigenesis.The synthetic peptides DG1/DG2 can specifically block this signaling pathway and may have therapeutic potential.

Article Snippet: Human umbilical vascular endothelial cells (HUVEC) and culture media were purchased from Cell Applications, Inc.

Techniques: In Vivo, Phospho-proteomics, Activity Assay, Invasion Assay, Incubation, Membrane, Control, Immunohistochemical staining, Staining, Protein-Protein interactions, Blocking Assay