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Vascular endothelial growth factor (VEGF) upregulates BCL-2 and inhibits apoptosis in human and murine mammary adenocarcinoma cells
Authors
Gagnon ML
Gimbrone MA
+18 more
Gorski DH
Hanahan D
Holmgren L
Jakeman LB
Katoh O
Kenyon BM
Krajewski S
Li WW
Liu R
Matsushita K
Mattsby-Baltzer I
Nor JE
Oltvai ZN
Pidgeon GP
Senger DR
Shen B-Q
Soker S
Thompson CB
Publication date
20 July 2001
Publisher
Nature Publishing Group
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PubMed
Abstract
Tumour progression is regulated by the balance of proliferation and apoptosis in the tumour cell population. To date, the role of vascular endothelial growth factor (VEGF) in tumour growth has been attributed to the induction of angiogenesis. VEGF has been shown to be a survival factor for endothelial cells, preventing apoptosis by inducing Bcl-2 expression. In both murine (4T1) and human (MDA-MB-231) metastatic mammary carcinoma cell lines, we found that VEGF upregulated Bcl-2 expression and anti-VEGF antibodies reduced Bcl-2 expression. These alterations in Bcl-2 expression were reflected by the levels of tumour cell apoptosis. VEGF resulted in reduced tumour cell apoptosis, whereas its inhibition with anti-VEGF neutralizing antibodies induced apoptosis directly in tumour cells. Therefore, in addition to its role in angiogenesis and vessel permeability, VEGF acts as a survival factor for tumour cells, inducing Bcl-2 expression and inhibiting tumour cell apoptosis. © 2001 Cancer Research Campaign http://www.bjcancer.co
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oai:figshare.com:article/10800...
Last time updated on 15/11/2023
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