results emphasize the significance of sds22 being a novel member of the neoplastic tumor suppressor gene course that links alterations in epithelial integrity with signaling pathways operating tumor metastasis. Among these, e3 ubiquitin scrib, dlg, and lgl have now been defined as neoplastic growth guards, whose loss cause structure over-growth associated with disruptions in cellular architecture and differentiation. Nevertheless, clones of scrib, dlg, or lgl survive badly when surrounded by wild type cells and are eradicated by cell apoptosis. This phenomenon is reminiscent of the multiple gene dependence on a standard cell to become tumorigenic and progress to malignancy. Drosophila imaginal discs have become a strong system to review the consequences of numerous genetic changes on discrete numbers of cells instantly next to wild-type neighboring cells, which closely resembles the nature of human cancer. Protein Phosphatase 1 is a member of one of the major Extispicy classes of serine/threonine protein phosphatases, which consists of a catalytic subunit and different regulatory subunits that goal the complex to specific areas and manage substrate specificity. PP1 term is reported to be dramatically lower in some human cancer cells and human PP1 interacts with breast cancer susceptibility protein BRCA1. Additionally, the PP1 inhibitor okadaic acid has been reported to act as a tumor promoter and can enhance migration and invasion of nonmetastatic LLC C8 cells, indicating that loss in PP1 may possibly subscribe to tumor formation and metastasis. However, genetic studies of PP1 function in vivo have been complicated by the presence of multiple homologs and its involvement in a wide selection of cellular processes in many organisms. Thus, PP1 regulatory subunits can provide a key to understanding the role of PP1 in cyst growth and metastasis. Sds22 is just a conserved, leucine prosperous repeat protein first defined as a regulatory subunit of PP1 that is needed for the completion of mitosis in yeast. Recently, one group discovered Drosophila sds22 as a regulator of epithelial order Lapatinib polarity. In this report, we show that, in addition to its role in cell polarity, sds22 is crucial for sustaining epithelial integrity, and that without sds22 cells become tumorigenic and invasive. Furthermore, sds22 over-expression may generally suppress the growth ofRasV12scrib cells. Finally, we show this one potential mechanism where sds22 prevents cell invasion and metastasis is through inhibition of myosin II and JNK exercise downstream of PP1. A previous study showed that sds22 is very important for epithelial cell shape and polarity. Given that loss of cell polarity often synergizes with activated Ras to stimulate tumefaction growth and invasion as seen in mutants, we first examined whether loss of sds22 could have an identical effect. We created null alleles of sds22 by imprecise excision of a nearby Pelement insertion in Drosophila, which also wiped another gene named CREG.