We realize that overexpression of Timp using ptc GAL4 clearly suppresses the invasive behavior of sds22 deficient cells in the wing disk, while overexpression of Timp alone causes no obvious problems. These data claim that MMP activity is important for the cell unpleasant behavior due to lack of sds22. Furthermore, we find that epithelial business defects, including an irregular apical ATP-competitive HDAC inhibitor folding across the A G border of the wing disk, aren’t rescued by overexpression of either puc or Timp, indicating that hyperactivity of myosin II might be sufficient to mediate this epithelial integrity defect. Stable epithelial integrity is necessary for normal tissue morphogenesis during development, and its reduction is often associated with cancer. The value of sds22 in controlling epithelial morphology is recently reported. Nevertheless, the step by step system of sds22 purpose and its role in cyst suppression haven’t been examined. By making new, null alleles of sds22 in Drosophila, we show for the first-time that sds22 is a new possible cyst suppressor gene that plays an integral role in the metastatic process. Consistent with the job of Grusche et al., our carcinoid syndrome results show that sds22 mutant cells eliminate epithelial organization, fail to distinguish typically, and undergo cell death. Beyond this, we show that sds22 mutant cells become invasive and migrate into neighboring regions, likely by increasing Matrix metalloprotease 1 secretion to degrade the basement membrane. Significantly, sds22 mutant cells undergo uncontrolled expansion when cell death is blocked or in cooperation with activated Ras. Alternatively, over-expression of sds22 may HCV NS3-4A protease inhibitor significantly delay tumor development of RasV12scrib / cells and control the phenotype in vivo, consistent with sds22 functioning as a tumor suppressor gene. Finally, our genetic research leads us to offer a novel type in which sds22 functions being an necessary good regulator of PP1 to restrict myosin II and JNK activity, thereby maintaining epithelial integrity and preventing proliferation and metastasis, which offers important new mechanistic insights in to tumefaction suppressor pathways. Most human tumors are derived from epithelial tissues and lack of epithelial integrity has been linked to tumor growth and invasion. Here, we provide evidence that sds22 is really a regulator of cell invasion and epithelial integrity, two key features of malignant epithelial cells. We have considered the possibility that the attack like behavior of sds22 / cells could be secondary to defects in cell death or cell adhesion. But, not all invasive sds22 / cells are Caspase 3 positive and blocking cell death does not suppress cell invasion behavior. Furthermore, we find while problems in cell adhesion frequently cause cells to spread into surrounding wild type cells, loss in sds22 often causes online migration.