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This article is part of the supplement: Abstracts of the 16th International Charles Heidelberger Symposium on Cancer Research

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Role of VEGF signalling in the regulation of KDR expression in endothelial and tumoral microenvironment

Jacinta Serpa123*, Cheila Torre123, Francisco Caiado123 and Sérgio Dias123

Author Affiliations

1 Centro de Investigação de Patobiologia Molecular, Instituto Português de Oncologia de Lisboa Francisco Gentil, EPE, Lisboa, Portugal

2 Instituto Gulbenkian de Ciência, Oeiras, Portugal

3 Centro de Estudos de Doenças Crónicas, Faculdade de Ciências Médicas, Universidade Nova de Lisboa, Lisboa, Portugal

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BMC Proceedings 2010, 4(Suppl 2):P34  doi:10.1186/1753-6561-4-S2-P34

The electronic version of this article is the complete one and can be found online at:

Published:24 September 2010

© 2010 Serpa et al; licensee BioMed Central Ltd.

Poster presentation

Vascular endothelial growth factor (VEGF) is the main regulator of angiogenesis. The paracrine VEGF signalling through KDR consists on the action of VEGF produced by a cell from different origins on KDR that is displayed on endothelial cells surface. In cancer, the functional significance of VEGF in tumour angiogenesis is very well documented but in the last 10 years a functional VEGF:KDR autocrine loop have been described in solid and haematological tumours, favouring disease burden by cell proliferation and motility promotion. However the regulation of KDR expression in endothelial and tumour cells remains rather unclear. The aim of the study is to evaluate the role of VEGF signalling in the expression of KDR in endothelial and tumour cells. This study was developed in endothelial cells (BEnd3, HUVEC and EPCs) and in colorectal carcinoma cell line HCT15. The regulation of KDR promoter was performed by Fire-fly luciferase reporter gene assays, using pGL3Basic deletion constructs of KDR promoter. The expression of KDR was analysed by FACS and immunofluorescence. The involvement of KDR in its own expression was confirmed using a neutralising anti-KDR. We observed that VEGF stimulates the activity of KDR promoter through KDR itself, in BEnd3, HUVEC, EPCs and HCT15; and through FLT1 in HUVEC. The results of promoter activity correlate with the concomitant expression of KDR. We can conclude that VEGF signalling pathway regulates the expression of VEGF receptor 2, KDR.