Cancer cells contribute to distinct malignant traits depending on their MYC and pJNK relative levels

Clonal analysis is common practice in Drosophila. In particular, induction of cell clusters carrying either loss-of-function alleles of neoplastic tumour suppressors or activated forms of oncogenes has successfully been exploited to study cooperative tumourigenesis in different organs. This strategy has allowed collecting a number of morphological and molecular details on the phenotypic traits associated with cancer progression. We previously identified MYC as a target of the Hippo pathway in Drosophila, and showed its expression is sufficient as to rescue the growth deficit of cells mutant for polarity genes, releasing their malignant nature. Here we expand on previous work, showing that cell growth and cell migration are separable traits in Drosophila epithelial cancers. While in situ cancer expansion is supported by MYC, migration depends on the AP-1 protein Fos. These proteins are strategically found at the crossroads of the Hippo, JNK and Ras/MAPK pathways, acknowledged by current literature as central players in cancer progression. Moreover, we show that growth and migration are mutually exclusive behaviours, with cells displaying different MYC and pJNK levels playing distinct roles in cancer evolution.