Requirement for Rac1 in a K-ras-induced lung cancer in the mouse

Joseph L. Kissil, Marita J. Walmsley, Linda Hanlon, Kevin M. Haigis, Carla F.Bender Kim, Alejandro Sweet-Cordero, Matthew S. Eckman, David A. Tuveson, Anthony J. Capobianco, Victor L.J. Tybulewicz, Tyler Jacks

Research output: Contribution to journalArticlepeer-review

143 Scopus citations


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.

Original languageEnglish (US)
Pages (from-to)8089-8094
Number of pages6
JournalCancer Research
Issue number17
StatePublished - Sep 1 2007
Externally publishedYes

ASJC Scopus subject areas

  • Oncology
  • Cancer Research


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