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Originally published online as doi:10.2353/ajpath.2008.070561 on December 28, 2007

Published online before print December 28, 2007
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(American Journal of Pathology. 2008;172:156-166.)
© 2008 American Society for Investigative Pathology
DOI: 10.2353/ajpath.2008.070561

A Critical Role for Rac1 in Tumor Progression of Human Colorectal Adenocarcinoma Cells

Carolina Espina*, María Virtudes Céspedes{dagger}, Miguel Angel García-Cabezas*{ddagger}, María Teresa Gómez del Pulgar*, Alicia Boluda*, Lourdes García Oroz*, Paloma Cejas*, Manuel Nistal*{ddagger}, Ramón Mangues{dagger} and Juan Carlos Lacal*

From the Translational Oncology Unit Consejo Superior de Investigaciones Cientificas-Universidad Autónoma de Madrid-La Paz,*Centro Nacional de Biotecnología, Madrid; Grup d’Oncogenesi i Antitumorals,{dagger}Laboratori d’Investigació Gastrointestinal, Institut de Recerca, Hospital de la Santa Creu i Sant Pau, Barcelona; and the Department of Pathology,{ddagger}Hospital Universitario La Paz, Madrid, Spain.

Colorectal adenocarcinoma is the second cause of cancer mortality in developed countries. Rac1 is a member of the family of Rho GTPases that regulates many intracellular signaling pathways, including those involved in tumorigenesis, invasion, and metastasis. We have investigated the role of Rac1 in colorectal tumor progression by genetic modification of the human colorectal adenocarcinoma cell line SW620 to either overexpress Rac1 or lack Rac1 expression. Tumor behavior was studied by orthotopic injection of stably modified cell lines into the cecal wall of athymic nude mice, a model that replicates the histopathological appearance and clinical behavior of human colorectal adenocarcinoma in humans. While overexpression of Rac1 resulted in an accelerated tumorigenic process, inducing a faster mortality rate, inhibition of Rac1 completely suppressed tumor formation. These results suggest that Rac1 plays a major role in colorectal adenocarcinoma progression. Finally, interference with Rac1 function may provide an important tool to block the malignant phenotype of colorectal adenocarcinoma cells.






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Copyright © 2008 by the American Society for Investigative Pathology.