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Carcinogenesis Advance Access originally published online on November 21, 2003
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Carcinogenesis, Vol. 25, No. 4, 535-539, April 2004
Carcinogenesis vol.25 no.4 © Oxford University Press 2004; all rights reserved.

CANCER BIOLOGY

Complex effects of Ras proto-oncogenes in tumorigenesis

Roberto Diaz1, Lluis Lopez-Barcons2,*, Daniel Ahn1,*, Antonio Garcia-Espana3, Andrew Yoon1, Jeremy Matthews1, Ramon Mangues4, Roman Perez-Soler2 and Angel Pellicer1,5

1 Department of Pathology and NYU Cancer Institute, New York University School of Medicine, New York, NY 10016, USA, 2 Department of Molecular Pharmacology, Albert Einstein College of Medicine, 1300 Morris Park Avenue, Bronx, NY 10461, USA, 3 Endocrinology Research Unit, Joan XXIII University Hospital, Rovira i Virgili University School of Medicine, Dr Mallafre i Guasch 4, Tarragona, Spain and 4 Laboratori d'Investigació Gastrointestinal, Institut de Recerca, Hospital de Sant Pau, E-08025 Barcelona, Spain

Ras proteins have been found mutated in about one-third of human tumors. In vitro, Ras has been shown to regulate distinct and contradictory effects, such as cellular proliferation and apoptosis. Nonetheless, the effects that the wild-type protein elicits in tumorigenesis are poorly understood. Depending on the type of tissue, Ras proto-oncogenes appear to either promote or inhibit the tumor phenotype. In this report, we treated wild-type and N-ras knockout mice with 3-methylcholanthrene (MCA) to induce fibrosarcomas and found that MCA is more carcinogenic in wild-type mice than in knockout mice. After injecting different doses of a tumorigenic cell line, the wild-type mice exhibited a shorter latency of tumor development than the knockouts, indicating that there are N-ras-dependent differences in the stromal cells. Likewise, we have analyzed B-cell lymphomas induced by either N-methylnitrosourea or by the N-ras oncogene in mice that over-express the N-ras proto-oncogene and found that the over-expression of wild-type N-ras is able to increase the incidence of these lymphomas. Considered together, our results indicate that Ras proto-oncogenes can enhance or inhibit the malignant phenotype in vivo in different systems.


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