scholarly journals Activation of Vascular Endothelial Growth Factor A Transcription in Tumorigenic Glioblastoma Cell Lines by an Enhancer with Cell Type-specific DNase I Accessibility

2002 ◽  
Vol 277 (22) ◽  
pp. 20087-20094 ◽  
Author(s):  
Yuxin Liang ◽  
Xiao-Yong Li ◽  
Edward J. Rebar ◽  
Peixiang Li ◽  
Yuanyue Zhou ◽  
...  
Keyword(s):  
Vascular Endothelial Growth Factor ◽  
Growth Factor ◽  
Cell Lines ◽  
Dnase I ◽  
Vascular Endothelial ◽  
Glioblastoma Cell ◽  
Cell Type ◽  
Cell Type Specific ◽  
Endothelial Growth Factor ◽  
Glioblastoma Cell Lines

scholarly journals Synthetic Triterpenoid CDDO-Me Inhibits Proliferation, Migration, and Invasion in GBM8401 and GBM8901

2020 ◽  
Vol 104 (3-4) ◽  
pp. 90-98 ◽  
Author(s):  
Chih-Hui Chang ◽  
Hung-Pei Tsai ◽  
Shih-Hsun Kuo ◽  
Joon-Khim Loh ◽  
Chien-Ju Lin ◽  
...  
Keyword(s):  
Vascular Endothelial Growth Factor ◽  
Growth Factor ◽  
Cyclin D1 ◽  
Cell Lines ◽  
Migration And Invasion ◽  
Vascular Endothelial ◽  
Glioblastoma Cell ◽  
Endothelial Growth Factor ◽  
Glioblastoma Cell Lines

Objectives: We determined the anticancer potency of CDDO-Me in glioblastoma cell lines and the underlying mechanisms in vitro. Summary: CDDO-Me is a synthetic triterpenoid with more potent anticancer and cancer preventive actions compared with the original triterpenoid CDDO. Methods: Two glioblastoma cell lines, GBM8401 and GBM8901, were utilized to test the effect of CDDO-Me on cell viability, cell migration, and cell invasion using the MTT, wound healing, and transwell migration assays, respectively. Additionally, Western blotting was used to determine the protein expression levels of N-cadherin, cyclin D1, and vascular endothelial growth factor. Results: At nanomolar concentrations, CDDO-Me inhibited proliferation, migration, and invasion in both cell lines. In addition, CDDO-Me exhibited a dose-dependent downregulation in the protein levels of N-cadherin, cyclin D1, and vascular endothelial growth factor in GBM8401 and GBM8901 cells. Conclusions: CDDO-Me exhibited anticancer effects at low nanomolar concentrations and should be considered as a potential chemotherapeutic agent for glioblastoma.

Sirolimus Toxicity and Vascular Endothelial Growth Factor Release From Islet and Renal Cell Lines

2007 ◽  
Vol 83 (12) ◽  
pp. 1635-1638 ◽  
Author(s):  
Matthew Laugharne ◽  
Sarah Cross ◽  
Sarah Richards ◽  
Charlotte Dawson ◽  
Laura Ilchyshyn ◽  
...  
Keyword(s):  
Vascular Endothelial Growth Factor ◽  
Growth Factor ◽  
Cell Lines ◽  
Renal Cell ◽  
Vascular Endothelial ◽  
Growth Factor Release ◽  
Endothelial Growth Factor ◽  
Renal Cell Lines ◽  
Factor Release

scholarly journals Thrombospondin-1 Is Downregulated by Anoxia and Suppresses Tumorigenicity of Human Glioblastoma Cells

2000 ◽  
Vol 191 (10) ◽  
pp. 1789-1798 ◽  
Author(s):  
Mirna Tenan ◽  
Giulia Fulci ◽  
Michele Albertoni ◽  
Annie-Claire Diserens ◽  
Marie-France Hamou ◽  
...  
Keyword(s):  
Vascular Endothelial Growth Factor ◽  
Growth Factor ◽  
Blood Vessels ◽  
Vascular Endothelial ◽  
Glioblastoma Cell ◽  
Glioblastoma Cells ◽  
Thrombospondin 1 ◽  
Natural Inhibitor ◽  
Endothelial Growth Factor

Angiogenesis, the sprouting of new capillaries from preexisting blood vessels, results from a disruption of the balance between stimulatory and inhibitory factors. Here, we show that anoxia reduces expression of thrombospondin-1 (TSP-1), a natural inhibitor of angiogenesis, in glioblastoma cells. This suggests that reduced oxygen tension can promote angiogenesis not only by stimulating the production of inducers, such as vascular endothelial growth factor, but also by reducing the production of inhibitors. This downregulation may significantly contribute to glioblastoma development, since we show that an increase in TSP-1 expression is sufficient to strongly suppress glioblastoma cell tumorigenicity in vivo.

Role of Vascular Endothelial Growth Factor/Vascular Permeability Factor in the Pathogenesis of Kaposi's Sarcoma-Associated Herpesvirus-Infected Primary Effusion Lymphomas

Blood ◽  
1999 ◽  
Vol 94 (12) ◽  
pp. 4247-4254 ◽  
Author(s):  
Yoshiyasu Aoki ◽  
Giovanna Tosato
Keyword(s):  
Vascular Endothelial Growth Factor ◽  
Growth Factor ◽  
Vascular Permeability ◽  
Cell Lines ◽  
Kaposi's Sarcoma ◽  
Vascular Endothelial ◽  
Vascular Permeability Factor ◽  
Permeability Factor ◽  
Endothelial Growth Factor ◽  
Primary Effusion Lymphomas

Abstract Primary effusion lymphomas (PELs), which are rare lymphomas associated with Kaposi's sarcoma-associated herpesvirus (or human herpesvirus-8) infection, present as malignant lymphomatous effusions in body cavities. Because PELs prefer liquid growth, we hypothesized that increased vascular permeability would be required for effusions to form. We found that the PEL cell lines BC-1, BCP-1, and BCBL-1 produce high levels of vascular endothelial growth factor/vascular permeability factor (VEGF/VPF). Reverse transcriptase-polymerase chain reaction analysis of RNA from the PEL cell lines amplified the 3 VEGF-secreted isoforms: VEGF/VPF121, VEGF/VPF145, and VEGF/VPF165. Two of the PEL cell lines expressed the VEGF/VPF receptor Flt-1, but VEGF/VPF did not stimulate proliferation in these cells. Most (13/14) control SCID/beige mice inoculated intraperitoneally with BCBL-1 cells and subsequently observed or treated with control antibodies developed effusion lymphoma of human cell origin with prominent bloody ascites. In contrast, none (0/9) of the mice treated with a neutralizing antihuman VEGF/VPF antibody developed ascites and effusion lymphoma. These results demonstrate that VEGF/VPF is critical to BCBL-1 growth as effusion lymphoma in mice and suggest that VEGF/VPF stimulation of vascular permeability may be critical to the pathogenesis of PELs.

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