Abstract：
: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.
journal_name
Cancer Resjournal_title
Cancer researchauthors
Kissil JL,Walmsley MJ,Hanlon L,Haigis KM,Bender Kim CF,Sweet-Cordero A,Eckman MS,Tuveson DA,Capobianco AJ,Tybulewicz VL,Jacks Tdoi
10.1158/0008-5472.CAN-07-2300subject
Has Abstractpub_date
2007-09-01 00:00:00pages
8089-94issue
17eissn
0008-5472issn
1538-7445pii
67/17/8089journal_volume
67pub_type
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