Decrease of endogenous vascular endothelial growth factor may not affect glioma cell proliferation and invasion.

Decrease of endogenous vascular endothelial growth factor may not affect glioma cell proliferation and invasion. Research Abstract Details 

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Decrease of endogenous vascular endothelial growth factor may not affect glioma cell proliferation and invasion. Abstract Text:

Xin Hong,Feng Jiang,Steven N Kalkanis,Zheng Gang Zhang,Xuepeng Zhang,Xuguang Zheng,Tom Mikkelsen,Hao Jiang,Michael Chopp,

Vascular endothelial growth factor (VEGF) is abundantly produced by glioma cells especially glioblastoma, the most malignant form of astrocytoma. VEGF, a well known angiogenic factor, acts in a paracrine fashion on endothelial cells to develop tumor vasculature. However, recent studies have found that several tumor cells express VEGF receptors, and an autocrine action of VEGF on tumor cells has been suggested. To test this hypothesis, three human glioma cell lines (U251n, U87 and A172) were checked for VEGF and VEGFR expression. These cells express 0.1-0.6 ng/ml VEGF165 in cell culture medium within 24 hours. Western blot analysis showed that these cells express all of the VEGF receptors, VEGFR-1/Flt-1, VEGFR-2/KDR, Neuropilin-1 (NRP-1) and Neuropilin-2(NRP-2), even though tyrosine kinase receptor VEGFR-2/KDR exhibited baseline levels of expression. VEGF expression was significantly down regulated by phosphorothioate oligodeoxynucleotide (PS-ODN) and VEGF RNAi transfection. However, VEGF RNAi transfection as well as VEGF and VEGFR2 neutralization antibody treatment did not decrease cell proliferation detected by MTT and CyQuant NF proliferation assay except that PS-ODN transfection caused a non-specific decrease on cell proliferation. VEGF RNAi transfection did not alter cell invasion, as demonstrated in a matrigel invasion assay. Matrix metalloproteinase-2 (MMP-2) and MMP-9, facilitating cell invasion and over expressed in glioma cells, were not altered by VEGF RNAi transfection, as shown by zymographic assays. Our data indicate that the decrease of endogenous VEGF expression may not affect glioma cell proliferation and invasion.

Decrease of endogenous vascular endothelial growth factor may not affect glioma cell proliferation and invasion. Publishing Authors By Initials

X Hong,F Jiang,SN Kalkanis,ZG Zhang,X Zhang,X Zheng,T Mikkelsen,H Jiang,M Chopp,

For similar peptides: intercellular signaling peptides and proteins: angiogenic proteins: vascular endothelial growth factors: vascular endothelial growth factor a research abstracts see: peptides: intercellular signaling peptides and proteins: angiogenic proteins: vascular endothelial growth factors: vascular endothelial growth factor a research

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Decrease of endogenous vascular endothelial growth factor may not affect glioma cell proliferation and invasion. Journal Published:

PUBLICATION TYPE: Research Support, Non-U.S. Gov

Journal: Journal of experimental therapeutics & oncology

VOLUME: 6

Page Numbers: 219-29

Journal Abbreviation: J. Exp. Ther. Oncol.

ISSN: 1359-4117

DAY: 3

MONTH: 12

YEAR: 2007

Decrease of endogenous vascular endothelial growth factor may not affect glioma cell proliferation and invasion. Information

Number of References:

LANGUAGE: eng

NlmUniqueID: 9604933

Decrease of endogenous vascular endothelial growth factor may not affect glioma cell proliferation and invasion. Keywords Mesh Terms:

KEYWORDS: Vascular Endothelial Growth Factor A

MESH TERMS: physiology

Chemical & Substance for Abstract: Decrease of endogenous vascular endothelial growth factor may not affect glioma cell proliferation and invasion. Information

Substance Name: Matrix Metalloproteinase 9

Registry Number: EC 3.4.24.35

Grant and Affiliation Information for Decrease of endogenous vascular endothelial growth factor may not affect glioma cell proliferation and invasion.

AFFILIATION: Department of Neurosurgery, Henry Ford Health Science Center, Detroit, MI 48202, USA.

Country: United States

AGENCY: United States NCI

GRANT: R01 CA100486

ACRONYM: CA

MEDLINETA: J Exp Ther Oncol

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