Analysis of cellular signals toward carcinogenesis and metastasis using genetically modified mice

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We analyzed Rb-heterozygous mice simultaneously lacking various Rb-related genes. We proved that Rb-deficient carcinogenesis is antagonized by cellular senescence and DNA damage response in a Ras-dependent manner. We also discovered that Rb inactivation upregulates number of genes involved in protein isoprenylation via E2F or SREBP leading to accelerated membrane trafficking of Ras. In addition, we discovered that RECK, an antagonistic downstream target of Ras, regulates beta1-integrin and EGFR signaling.