Loss of the emei tumor suppressor promotes tumorigenesis via the JNK and Hippo pathway

Mutations in the Ras oncogene are the most frequently cancer alterations, occurring in more than 30% of all human cancers. The failures in the development of successful clinical inhibitors against Ras have made Ras as a “undruggable” target. The major reason is lack of a systematic understanding of oncogenic cooperation between Ras activation and mutation of related tumor suppressor genes.1 The genetic techniques available in the Drosophila melanogaster allow analysis of the behavior of cells with distinct mutations, making this the ideal model organism to dissect oncogenic cooperation induced tumorigenesis.2 The exact same mutation, e.g., RasV12, was mimicked in the Drosophila, which enables us to perform large scale genetic screens, aiming to unearth novel tumor suppressors that can synergistically enhance RasV12-related tumor growth.