Journal
CANCER RESEARCH
Volume 67, Issue 17, Pages 8089-8094Publisher
AMER ASSOC CANCER RESEARCH
DOI: 10.1158/0008-5472.CAN-07-2300
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Funding
- Medical Research Council [MC_U117527252] Funding Source: researchfish
- Medical Research Council [MC_U117527252] Funding Source: Medline
- NCI NIH HHS [P30 CA14051] Funding Source: Medline
- MRC [MC_U117527252] Funding Source: UKRI
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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.
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