It will be important to further these findings using various ovarian cancer cell lines, especially those who aren’t dependent on PI3K/Akt for invasion and migration. However, in further assistance of our results, a current study showed a relationship between decreased invasion in SKOV 3 cells and decreased phosphorylated Akt levels. Also, (-)-MK 801 the regulation of uPA expression and activity by the PI3K/Akt process that we showed confirmed previously published results. Finally, Venugopal et a-l. showed in a in vivo study that lcd PAI 1 was up controlled in Akt deficient rats, which may attenuate the PI3K/Akt signaling pathway. Possible initiators of the plasminogen activator system that could be altered by the PI3K/Akt pathway are IGF 1 and insulin. Increased levels of IGF 1 have already been related to an increased risk in devel-opment of ovarian cancer. The relationship of insulin is worth addressing since obesity and metabolic syndrome have been related to various cancers. Recently, it had been found that insulin induced PAI 1 levels in 3T3L1 adipocytes were improved by treatment using the PI3K inhibitor LY294002. Applying IGF 1 and insulin, which are both proven to increase uPA levels, in a wound caused Immune system migration analysis, we found that these growth factors improved SKOV 3 cell migration and this increase was attenuated upon treatment with LY294002. Overall, the book finding here is that PI3K/Akt action adjusts cell migration as a result of improvements in both PAI 1 and uPA expression in SKOV 3 cells, showing that the PI3K/Akt signaling process negatively regulates PAI 1 expression although it up regulates uPA expression, and this action is further modulated by IGF 1 and insulin. Nevertheless, the low traditional functions for PAI 1, including expansion, cell adhesion, angiogenesis, apoptosis and cell signaling, are most likely contributing to the harmful role performed by PAI 1 and why this inhibitor GW0742 is of a grim prognosis in several cancers. Based on the experimental end points that individuals measured, the decrease in invasion and SKOV 3 migration implies an even more positive situation to avoid further metastasis. Nevertheless, because it is well recognized that elevated levels of PAI 1 are associated with a prognosis in ovarian cancer, this obvious contradiction seen here may be better understood by evoking a mixture of both conventional and the nontraditional characteristics of PAI 1. The original function of PAI 1 will be to prevent uPA and thus avoid plasmin generation and matrix degradation. Our results are supported by work demonstrating that IGF 1 affects growth and invasion in cervical and ovarian cancer cells through activation of Akt and ERK1/2, resulting in a growth in uPA activity in ovarian cancer.