We observe that overexpression of Timp using ptc GAL4 clearly suppresses the behavior of sds22 deficient cells in the wing disk, while overexpression of Timp alone causes no obvious defects. These data claim that MMP activity is crucial for the cell unpleasant behavior caused by lack of sds22. Moreover, we find that epithelial firm defects, including an abnormal apical k63 ubiquitin folding over the A P boundary of the wing disk, are not rescued by over-expression of either puc or Timp, suggesting that hyperactivity of myosin II might be sufficient to mediate this epithelial integrity defect. Secure epithelial integrity is necessary for normal muscle morphogenesis all through development, and its reduction is usually connected with cancer. The importance of sds22 in regulating epithelial morphology has been recently reported. However, the detail by detail process of sds22 function and its role in tumor suppression have not been examined. By creating new, null alleles of sds22 in Drosophila, we show for the first time that sds22 is a new possible tumor suppressor gene that plays a key role in the metastatic process. Consistent with the task of Grusche et al., our Cellular differentiation results show that sds22 mutant cells lose epithelial organization, fail to differentiate normally, and undergo cell death. Beyond this, we show that sds22 mutant cells become invasive and migrate into neighboring areas, likely by increasing Matrix metalloprotease 1 secretion to degrade the basement membrane. Significantly, sds22 mutant cells endure uncontrolled expansion when cell death is blocked or in cooperation with activated Ras. However, overexpression of sds22 could Tipifarnib ic50 significantly delay tumor growth of RasV12scrib / cells and reduce the scrib phenotype in vivo, in keeping with sds22 functioning as a tumor suppressor gene. Finally, our genetic evidence leads us to offer a novel model in which sds22 functions being an crucial positive regulator of PP1 to limit myosin II and JNK activity, therefore maintaining epithelial integrity and preventing proliferation and metastasis, which provides significant new mechanistic insights in to tumefaction suppressor pathways. Many human tumors are derived from epithelial tissues and loss in epithelial integrity has been connected to tumor growth and invasion. Here, we provide evidence that sds22 is a regulator of cell invasion and epithelial integrity, two important traits of malignant epithelial cells. We’ve considered the possibility that the invasion like behavior of sds22 / cells might be secondary to defects in cell death or cell adhesion. Nevertheless, not all invasive sds22 / cells are Caspase 3 good and blocking cell death does not suppress cell invasion behavior. Furthermore, we find while defects in cell adhesion often cause cells to spread in to surrounding wild type cells, lack of sds22 often causes online migration.