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Overexpression of vascular endothelial growth factor induces cell transformation in cooperation with fibroblast growth factor 2

Oncogene volume 14, pages 463–471 (1997)Cite this article

Abstract

Vascular endothelial growth factor (VEGF) is a family of homodimeric proteins produced from a single gene by alternative splicing of the VEGF transcript. VEGF induces in vivo angiogenesis and vascular permeability. We have recently demonstrated that VEGF is an autocrine growth factor for retinal pigment epithelial (RPE) cells. To further understand the role of VEGF, we overexpressed VEGF in rat RPE cells. The transfected cells exhibited a growth advantage in vitro and an increased response to the mitogenic effect of fibroblasts growth factor-2 (FGF-2), and formed colonies in soft agar upon FGF-2 addition. Moreover, analysis of FGF-receptors evidenced a dramatic increase in FGFR-1 mRNA and protein level, supporting the hypothesis that this receptor mediates the transforming effect of FGF-2. These results reveal that the oncogenic role of VEGF is exerted through a cross regulation between VEGF and FGF signal transduction pathways.

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Author notes

  1. François Malecaze

    Present address: Laboratoire d'Ophtalmologie, Hopital Purpan, Toulousse, France

Authors and Affiliations

  1. Laboratoire de Biologie Moléculaire Eucaryote, UPR 9006 Centre National de la Recherche Scientifique, 118, Route de Narbonne, Toulouse cedex, 31062, France

    Marina Guerrin, François Malecaze & Jean Plouët

  2. Institut National de la Santé et de la Recherche Medicale U211, Institut de Biologie, Nantes cedex, 44035, France

    Emmanuel Scotet & Elisabeth Houssaint

Authors
  1. Marina Guerrin
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  2. Emmanuel Scotet
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  3. François Malecaze
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  4. Elisabeth Houssaint
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  5. Jean Plouët
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Guerrin, M., Scotet, E., Malecaze, F. et al. Overexpression of vascular endothelial growth factor induces cell transformation in cooperation with fibroblast growth factor 2. Oncogene 14, 463–471 (1997). https://doi.org/10.1038/sj.onc.1200846

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  • DOI: https://doi.org/10.1038/sj.onc.1200846

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