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Nucleic Acids Research, 2003, Vol. 31, No. 19 5789-5804
© 2003 Oxford University Press

Integrated transcriptome analysis of the cellular mechanisms associated with Ha-ras-dependent malignant transformation of the human breast epithelial MCF7 cell line

Franck Gadal*, Christophe Bozic1, Céline Pillot-Brochet1, Sophie Malinge1, Sarah Wagner1, Aurélie Le Cam1, Laurent Buffat1, Michel Crepin and François Iris2

Unité Inserm U 553, Hôpital St Louis, 75010 Paris, France and Université Paris 13, France, 1 Valigen, Tour Neptune, 92086 Paris La Défense, France and 2 Ecole Centrale de Paris, Grande voie des vignes, 92295 Chatenay Malabry, France

*To whom correspondence should be addressed. Tel/Fax: +33 1 48 38 77 20; Email: fgadal{at}club-internet.fr

To understand the cellular mechanisms of malignant transformation induced by constitutive activation of the ras oncogene (Ha-ras), we used a subtractive hybridization method (VGIDTM) together with an integrative analytical procedure based upon literature databases in the form of extensive interaction graphs. We found 166 over- and under-expressed genes which, in the human MCF7-ras breast epithelial cell line, are involved in the different aspects of tumoral transformation such as defined signaling pathways, cellular growth, protection against apoptosis, extracellular matrix and cytoskeleton remodeling. Integrative analysis led to the construction of a physiological model defining cross-talk and signaling pathway alterations which explicitly suggested mechanisms directly involved in tumor progression. The model further suggested points and means of intervention which could induce cell death in Ha-ras-transformed cells specifically. These hypotheses were directly tested in vitro and found to be largely correct, hence indicating that these new analytical and technological approaches allow the discovery of pathology-associated cellular mechanisms and physiologically defined targets leading to phenotype-specific pharmacological interventions.


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F Gadal, A Starzec, C Bozic, C Pillot-Brochet, S Malinge, V Ozanne, J Vicenzi, L Buffat, G Perret, F Iris, et al.
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