Decreased tumorigenesis in mice with a Kras point mutation at C118

Lu Huang, John Carney, Diana M. Cardona and Christopher M. Counter ()
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Lu Huang: Duke University Medical Center
John Carney: Duke University Medical Center
Diana M. Cardona: Duke University Medical Center
Christopher M. Counter: Duke University Medical Center

Nature Communications, 2014, vol. 5, issue 1, 1-10

Abstract: Abstract KRAS, NRAS or HRAS genes are mutated to encode an active oncogenic protein in a quarter of human cancers. Redox-dependent reactions can also lead to Ras activation in a manner dependent upon the thiol residue of cysteine 118 (C118). Here, to investigate the effect of mutating this residue on tumorigenesis, we introduce a C118S mutation into the endogenous murine Kras allele and expose the resultant mice to the carcinogen urethane, which induces Kras mutation-positive lung tumours. We report that Kras+/C118S and KrasC118S/C118S mice develop fewer lung tumours. Although the KrasC118S allele does not appear to affect tumorigenesis when the remaining Kras allele is conditionally oncogenic, there is a moderate imbalance of oncogenic mutations favouring the native Kras allele in tumours from Kras+/C118S mice treated with urethane. We conclude that the KrasC118S allele impedes urethane-induced lung tumorigenesis.

Date: 2014
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DOI: 10.1038/ncomms6410

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