Abstract
Abstract : Our goal in this project was to characterize Cdk5 as a tumor suppressor gene in non-small cell lung cancer. We sought to examine this function in the context of two of the major oncogene-driven mechanisms of lung carcinogenesis, activation of Kras and Egfr. To accomplish this, we have generated a novel inducible autochthonous lung cancer mouse model, CE- Cdk5f/f, in which mutant Egfr expression is doxycycline inducible, and Cdk5 ablation is mediated by nasally instilled adenoviral-Cre. We also introduced Cdk5f/f into a KC lung cancer model, in which Kras is activated, and Cdk5 is simultaneously ablated, by adenoviral-Cre. In both models, ablation of Cdk5 resulted in significant acceleration of lung tumorigenesis. Our confirmation in two in vivo models of clinically germane oncogene-driven lung cancer, involving the oncogenes EGFRL858R and KrasG12D, that Cdk5 deletion accelerates or promotes tumorigenesis, strongly indicate that Cdk5 behaves as a tumor suppressor in lung adenocarcinoma tumorigenesis.
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