Vascular endothelial growth factor (VEGF) upregulates BCL-2 and inhibits apoptosis in human and murine mammary adenocarcinoma cells

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 endotheli...

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Bibliographic Details
Published in:British journal of cancer 2001-07, Vol.85 (2), p.273-278
Main Authors: Pidgeon, G P, Barr, M P, Harmey, J H, Foley, D A, Bouchier-Hayes, D J
Format: Article
Language:English
Subjects:
Adenocarcinoma - pathology
Angiogenesis
Animals
Antibodies
Apoptosis
Apoptosis - physiology
Biological and medical sciences
Biomedical and Life Sciences
Biomedicine
Breast Neoplasms - pathology
Cancer Research
Cancer therapies
Carcinogenesis, carcinogens and anticarcinogens
Cell culture
Cell death
Drug Resistance
Endothelial Growth Factors - physiology
Epidemiology
General aspects
Humans
In Situ Nick-End Labeling
Lymphokines - physiology
Mammary Neoplasms, Experimental - pathology
Medical research
Medical sciences
Metastasis
Mice
Molecular Medicine
Oncology
Penicillin
Permeability
Proteins
Proto-Oncogene Proteins c-bcl-2 - immunology
Proto-Oncogene Proteins c-bcl-2 - metabolism
Radiation
Regular
regular-article
Tumor Cells, Cultured
Tumors
Up-Regulation - immunology
Up-Regulation - physiology
Vascular endothelial growth factor
Vascular Endothelial Growth Factor A
Vascular Endothelial Growth Factors
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Summary: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.com
ISSN:0007-0920
1532-1827
DOI:10.1054/bjoc.2001.1876