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Requirement for Rac1 in a K-ras–Induced Lung Cancer in the Mouse

¹ Program in Molecular Oncogenesis, The Wistar Institute, Philadelphia, Pennsylvania; ² Division of Immune Cell Biology, National Institute for Medical Research, The Ridgeway, Mill Hill, London, United Kingdom; ³ Department of Biology and ⁴ Howard Hughes Medical Institute, Massachusetts Institute of Technology, Cambridge, Massachusetts; ⁵ Department of Pediatrics, Division of Cancer Biology, Stanford University School of Medicine, Stanford, California; and ⁶ Cambridge Research Institute/Cancer Research United Kingdom, University of Cambridge, Department of Oncology, Cambridge, United Kingdom

Requests for reprints: Joe Kissil, Molecular and Cellular Oncogenesis Program, Wistar Institute, Philadelphia, PA 19104. Phone: 215-898-3874; E-mail: jkissil{at}wistar.org or Tyler Jacks, Howard Hughes Medical Institute, Department of Biology, Massachusetts Institute of Technology, Cambridge, MA 02139; E-mail: tjacks{at}mit.edu.

Given the prevalence of Ras mutations in human cancer, it is critical to understand the effector pathways downstream of oncogenic Ras leading to transformation. To directly assess the requirement for Rac1 in K-ras–induced tumorigenesis, we employed a model of lung cancer in which an oncogenic allele of K-ras could be activated by Cre-mediated recombination in the presence or absence of conditional deletion of Rac1. We show that Rac1 function is required for tumorigenesis in this model. Furthermore, although Rac1 deletion alone was compatible with cell viability and proliferation, when combined with K-ras activation in primary epithelial cells, loss of Rac1 caused a profound reduction in proliferation. These data show a specific requirement for Rac1 function in cells expressing oncogenic K-ras. [Cancer Res 2007;67(17):8089–94]

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