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Human colorectal cancer (CRC) is a major cause of cancer mortality and frequently harbors activating mutations in the KRAS gene. To understand the role of oncogenic KRAS in CRC, we engineered a mouse model of metastatic CRC that harbors an inducible oncogenic Kras allele ( Kras   mut  ) and conditional null alleles of Apc and Trp53 (iKAP). The iKAP model recapitulates tumor progression from adenoma through metastases. Whole-exome sequencing revealed that the Kras   mut  allele was heterogenous in primary tumors yet homogenous in metastases, a pattern consistent with activated Kras   mut  signaling being a driver of progression to metastasis. System-level and functional analyses revealed the TGF-β pathway as a key mediator of Kras   mut  -driven invasiveness. Genetic extinction of Kras   mut  resulted in specific elimination of the Kras   mut  subpopulation in primary and metastatic tumors, leading to apoptotic elimination of advanced invasive and metastatic disease . This faithful CRC model provides genetic evidence that Kras   mut  drives CRC invasion and maintenance of metastases.

Oncogenic Kras drives invasion and maintains metastases in colorectal cancer