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Vol. 13, Issue 11, 4029-4044, November 2002
and
*Lady Davis Institute for Medical Research of the Sir Mortimer B. Davis Jewish General Hospital, Departments of Medicine, Oncology,
Pharmacology/Therapeutics and McGill Centre for Translational Research
in Cancer, McGill University, Montreal, Quebec, H3T 1E2, Canada;
Interactions between cancer cells and their microenvironment
are critical for the development and progression of solid tumors. This
study is the first to examine the role of all members of the ErbB
tyrosine kinase receptors (epidermal growth factor receptor [EGFR],
ErbB-2, ErbB-3, or ErbB-4), expressed singly or as paired receptor
combinations, in the regulation of angiogenesis both in vitro and in
vivo. Comparison of all receptor combinations reveals that EGFR/ErbB-2
and ErbB-2/ErbB-3 heterodimers are the most potent inducers of vascular
endothelial growth factor (VEGF) mRNA expression compared with
EGFR/ErbB-3, EGFR/ErbB-4, ErbB-2/ErbB-4, and ErbB-3/ErbB-4.
Immunohistochemistry of tumor xenografts overexpressing these
heterodimers shows increased VEGF expression and remarkably enhanced
vascularity. Enhanced VEGF expression is associated with increased VEGF
transcription. Deletional analysis reveals that ErbB-mediated
transcriptional up-regulation of VEGF involves a hypoxia-inducible
factor 1-independent responsive region located between
nucleotides Investigative Treatment Division, National Cancer Center
Research Institute East, Chiba, 277-8577 Japan; Centre
de Biochimie, Centre National de la Recherche Scientifique-Unité
Mixte Recherche 6543, Université de Nice, 06108 Nice, France; and
§Friedrich Miescher-Institute, CH-4002 Basel, Switzerland
88 to 66 of the VEGF promoter. Mutational analysis
reveals that the Sp-1 and AP-2 transcription factor binding elements within this region are required for up-regulation of VEGF by
heregulin 
1 and that this up-regulation is dependent on the activity
of extracellular signal-related protein kinases. These results
emphasize the biological implications of cell signaling diversity among
members of the ErbB receptor family in regulation of the tumor microenvironment.
Corresponding author. E-mail address:
malaou{at}po-box.mcgill.ca.
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