Phosphorylation of Bad by AKT prevents this interaction rebuilding the anti apoptotic function of BclXL. Upon presenting its cell surface urokinase receptor, uPA initiates plasminogen in-to plasmin to help tumor cell invasion and extracellular matrix degradation. Along with proteolytic activity and legislation, uPAR, PAI 1 and uPA are implicated in cell signaling pathways controlling cell proliferation, migration and invasion. The PI3K/Akt cell signaling pathway is implicated in cell migration and invasion. The PI3K/Akt pathway adjusts uPA expression, selective inhibition natural compound library of the pathway in numerous cell types lowers uPA expression and/ or activity with a subsequent decline in cell invasion. Urokinase itself-has been reported to promote PI3K activity and activates the downstream effectors Akt and Rac1. Inversely, antisense uPA in glioblastoma cells causes a decrease both in wound migration and in action. Conversely, looking at PAI 1 degrees, both hypoxia induced PAI 1 expression and nerve growth factor induced PAI 1 expression can be inhibited by PI3K inhibitors. A connection between phosphorylated Akt and PAI 1 was recently Eumycetoma demonstrated in aortic endothelial cells in the PAI 1 knock-out mouse, which showed increased phosphorylated Akt levels in comparison to wild type aortic endothelial cells. Furthermore, equally insulin like growth factor 1 and insulin modulate expression of uPA and PAI 1 through PI3K/Akt in breast cancer cells and in adipocytes. Insulin and igf 1 are involved in cell proliferation, survival and cell migration, therefore, their interaction with PI3K/Akt and the improvements in expression of uPA and PAI 1 are being studied in several different disease controls. The PI3K pathway is essential in ovarian carcinogenesis. Akt has demonstrated an ability to be amplified or over expressed in ovarian cancer, meaning that it also has a job in ovarian carcinogenesis. PI3K is constitutively activated inside the SKOV 3 ovarian cancer cell line. The PI3K/Akt pathway is an important signaling pathway to examine in the context of ovarian cancer and in relation to both uPA phrase and PAI 1. Utilizing the SKOV 3 ovarian cancer cell line as a for ovarian cancer in in-vitro migration assays, we sought to better comprehend the relationship of the PI3K/Akt path to PAI 1 and uPA. This study describes the results of a selection of signaling pathway inhibitors on both basal unstimulated SKOV3 and on insulin and IGF 1 addressed SKOV 3 cell migration. SKOV 3 cells were obtained from the University of North Carolina Tissue Culture Facility in the Lineberger Comprehensive Cancer Center and preserved as monolayer culture in minimal Dulbeccos altered Eagles medium supplemented with ten percent fetal bovine serum and one of the antibiotic/antimycotic in a humidified chamber with five minutes CO2 at 3-7 C.