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Epithelial polarity genes are important for maintaining tissue architecture, and regulating growth. The  Drosophila  neoplastic tumor suppressor gene  scribble (scrib)  belongs to the basolateral polarity complex. Loss of  scrib  results in disruption of its growth regulatory functions, and downregulation or mislocalization of Scrib is correlated to tumor growth. Somatic  scribble  mutant cells ( scrib  - ) surrounded by wild-type cells undergo apoptosis, which can be prevented by introduction of secondary mutations that provide a growth advantage. Using genetic tools in  Drosophila , we analyzed the phenotypic effects of loss of  scrib  in different growth promoting backgrounds. We investigated if a central mechanism that regulates cell adhesion governs the growth and invasive potential of  scrib  mutant cells. Here we show that increased proliferation, and survival abilities of  scrib  -  cells in different genetic backgrounds affect their differentiation, and intercellular adhesion. Further, loss of  scrib  is sufficient to cause reduced cell survival, activation of the JNK pathway and a mild reduction of cell adhesion. Our data show that for  scrib  cells to induce aggressive tumor growth characterized by loss of differentiation, cell adhesion, increased proliferation and invasion, cooperative interactions that derail signaling pathways play an essential role in the mechanisms leading to tumorigenesis. Thus, our study provides new insights on the effects of loss of  scrib  and the modification of these effects via cooperative interactions that enhance the overall tumorigenic potential of  scrib  deficient cells.

Loss of Cell Adhesion Increases Tumorigenic Potential of Polarity Deficient Scribble Mutant Cells